Zhongguo Zhongyao Zazhi最新文献

{"title":"[Acteoside ameliorates lung injury in septic mice by suppressing neutrophil extracellular trap formation through ROS/MAPK/PAD4 signaling pathway].","authors":"Kai Chen, Yong-Yan Jia, Qi Zheng, Meng-di Shao, Ke-Jia Zhang, Ya Gao, Yan-Hui Zhu","doi":"10.19540/j.cnki.cjcmm.20260515.801","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260515.801","url":null,"abstract":"<p><p>This study investigated the effects of acteoside on neutrophil extracellular traps(NETs) formation in the lung tissue of septic mice via the reactive oxygen species(ROS)/mitogen-activated protein kinase(MAPK)/peptidylarginine deiminase 4(PAD4) signaling pathway. A sepsis model was established by intraperitoneal injection of lipopolysaccharide(LPS). Mice were administered high-, medium-, or low-dose acteoside by gavage, and N-acetyl-L-cysteine(NAC) was used as a positive control. The 96 h survival rate of mice was observed. Pathological changes in lung tissue were evaluated by HE staining. Total cell count and total protein content in bronchoalveolar lavage fluid(BALF) were determined. Levels of tumor necrosis factor-α(TNF-α), interleukin(IL)-1β, and IL-6 in BALF were measured by ELISA. Intracellular ROS levels in BALF cells were detected by flow cytometry. Cell-free DNA(cf-DNA) content in BALF was quantified using a commercial assay kit. Immunofluorescence staining was performed to detect the expression of myeloperoxidase(MPO) and citrullinated histone H3(CitH3) in lung tissue. Protein expression levels of phosphorylated extracellular signal-regulated kinase(p-ERK)/ERK, phosphorylated p38 MAPK(p-p38)/p38, phosphorylated c-Jun N-terminal kinase(p-JNK)/JNK, PAD4, MPO, and CitH3/H3 in lung tissue were evaluated by Western blot. The results showed that acteoside at doses of 100 and 200 mg·kg~(-1) markedly increased the survival rate of septic mice, reduced the leukocyte count and total protein concentration, decreased the levels of inflammatory cytokines including TNF-α, IL-6, and IL-1β in BALF, and alleviated lung inflammation in septic mice. Acteoside dose-dependently decreased intracellular ROS levels in BALF cells and downregulated the protein expression of pERK/ERK, p-p38/p38, and p-JNK/JNK in the lung tissue of septic mice. In addition, acteoside treatment reduced cf-DNA content in BALF, decreased the co-localized fluorescence intensity of MPO and CitH3 in lung tissue, and downregulated the protein expression of PAD4, MPO, and CitH3, suggesting that acteoside inhibited sepsis-induced NETs formation in lung tissue. These findings indicate that acteoside mitigates sepsis-induced acute lung injury by suppressing NETs formation through regulation of the ROS/MAPK/PAD4 signaling pathway.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 17","pages":"5009-5017"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Chemical constituents from scammony resin].","authors":"Ting He, Xue-Rui An, Wei Liu, Jing-Jing Qi, Tao Yuan","doi":"10.19540/j.cnki.cjcmm.20260519.201","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260519.201","url":null,"abstract":"<p><p>The chemical constituents of the Uygur medicinal material scammony resin were investigated using a combination of normal-phase silica gel chromatography, reversed-phase ODS chromatography, Sephadex LH-20 chromatography, and semi-preparative high-performance liquid chromatography(HPLC). Twenty-seven compounds were isolated and identified from its methanol extract. Among them, compound 1 was a new compound and was named scammonoid A(1). The remaining twenty-six known compounds were identified as dehydroabietic acid(2), 7-oxo-dehydroabietic acid(3), 7β-hydroxy-dehydroabietic acid(4), 7α-hydroxydehydroabietic acid(5), 15-hydroxy-dehydroabietic acid(6), 15-methoxy-dehydroabietic acid(7), 7-oxo-15-hydroxy-dehydroabietic acid(8), 7α,15-dihydroxy-dehydroabietic acid(9), dabeshanensin L(10), cephasinene B(11), abietic acid(12), 12-methoxy-7,13-abietadien-18-oic acid(13), 12-oxoabieta-7,13-dien-18-oic acid(14), 7-oxo-13β-hydroxyabiet-8(14)-en-18-oic acid(15), aquilarabietic acid B(16), 9,13β-epidioxy-8(14)-abieten-18-oic acid(17), karamatsuic acid(18),(1 R,4 aR,5 R,8 aR)-6-formyl-1, 4a-dimethyl-5-( 4-methyl-3-oxopentyl)-1, 2, 3, 4, 4a, 5, 8, 8a-octahydronaphthalene-1-carboxylic acid(19), 16-nor-15-oxodehydroabietic acid(20), 8(14)-podocarpen-13-on-18-oic acid(21), abiesanordine E(22), junicedric acid(23), methyl-entlabd-8(17)-18-oic acid-15-oate(24), ent-isopimara-8,15-dien-7-oxo-18-oic acid(25), ent-isopimar-8(14),15-dien-19-oic acid(26), and isopimaric acid(27), all of which were isolated from scammony resin for the first time. In vitro cyclooxygenase-2(COX-2) inhibitory assays showed that compounds 2, 4, 6, 15, 16, and 21 exhibited certain inhibitory activity. This study provides a chemical reference for the quality evaluation and further development and utilization of scammony resin.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 17","pages":"4961-4971"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Ergosterol peroxide inhibits proliferation of breast cancer MDA-MB-231 cells via synergistic ferroptosis and mitochondrial-dependent apoptosis mediated by p53 signaling pathway].","authors":"Li-Man Hou, Ran Luo, Qi Wang, Lu Wang, Si-Qi Deng, Ming Bu, Yu Lin","doi":"10.19540/j.cnki.cjcmm.20260603.802","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260603.802","url":null,"abstract":"<p><p>Based on proteomic methods, this paper aims to explore the target and action mechanism of ergosterol peroxide(EP) against triple-negative breast cancer. The effect of EP on the viability of breast cancer MDA-MB-231 cells was detected by the MTT method. The effect of EP on apoptosis, mitochondrial membrane potential(detected by JC-1), reactive oxygen species(ROS), and the cell cycle of MDA-MB-231 cells was detected by flow cytometry. The subcellular localization and differentially expressed proteins of MDA-MB-231 cells treated with EP were obtained by proteomic technology based on tandem mass spectrometry. GO function and KEGG enrichment analysis were conducted through the eggNOG and KAAS databases. A protein-protein interaction(PPI) network was constructed via the STRING database. Malondialdehyde(MDA), superoxide dismutase(SOD), and glutathione(GSH) concentrations, as well as iron contents, were measured using a microplate reader. A Western blot was performed to detect the expression of relevant proteins, and molecular docking was used to validate the binding affinity of EP to relevant core target proteins. MTT results demonstrate that EP significantly inhibits MDA-MB-231 cell viability in a time-and concentration-dependent manner. The results of flow cytometry show that after MDA-MB-231 cells are treated with EP of 10, 20, and 40 μmol·L~(-1) for 48 hours, the total apoptosis rate of the cells increases significantly. The mitochondrial membrane potential decreased significantly; the level of ROS increased significantly; cell cycle arrest occurred in the G_0/G_1 phase. Proteomic results demonstrate that compared with those in the blank group, 895 differentially expressed proteins are identified in the EP group, with 326 upregulated proteins and 569 downregulated proteins. Bioinformatics pathway enrichment analysis indicates significant enrichment of ferroptosis and tumor protein p53 signaling pathways among these differentially expressed proteins, suggesting that EP may exert an inhibitory effect on MDA-MB-231 cell proliferation through multiple pathways. The Western blot results show that the protein expressions of cytochrome C(Cyt C), B-cell lymphoma-2(Bcl-2)-associated X protein(Bax), cleaved cysteine-aspartic acid protease-7(cleaved caspase-7), heme oxygenase 1(HOMX1), p53, and p21 protein are increased in MDA-MB-231 cells treated with EP. In contrast, the protein expressions of Bcl-2, solute carrier family 7 member 11(SLC7A11), glutathione peroxidase 4(GPX4), regulatory subunit of glutamate-cysteine ligase(GCLM), p62 protein, and cyclin-dependent kinase 4(CDK4) are decreased. The above findings suggest that EP may promote apoptosis in MDA-MB-231 breast cancer cells by regulating the p53 signaling pathway and inducing ferroptosis.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 18","pages":"5342-5352"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Mechanism of sensitization and clinical efficacy of ceftazidime combined with Tanreqing Injection in treating drug-resistant Pseudomonas aeruginosa].","authors":"Shuo Yang, Lu Li, Blažekovi Biljana, Bin Wang, Hai-Qiang Wang, Shuang Liu, Yi Wang","doi":"10.19540/j.cnki.cjcmm.20260519.501","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260519.501","url":null,"abstract":"<p><p>Acute respiratory infection(ARI) caused by drug-resistant Pseudomonas aeruginosa(PA) is increasingly prevalent, posing a serious challenge to public health. To address this clinical issue, combination strategies involving antibiotics and adjuvants have garnered considerable attention. Tanreqing Injection(TRQ), a commonly used traditional Chinese medicine compound preparation in the clinical treatment of ARI, has been preliminarily shown to enhance the antibacterial efficacy of ceftazidime(CAZ) against drug-resistant PA. To elucidate the underlying sensitization mechanism, this study first employed stimulated emission depletion(STED) microscopy to observe morphological alterations in drug-resistant PA following drug administration. Subsequently, transcriptomic analysis was performed to identify differentially expressed genes(DEGs) in PA before and after TRQ treatment. Ethidium bromide(EtBr) accumulation was conducted to assess efflux pump function. N-phenyl-1-naphthylamine(NPN) uptake was conducted to assess outer membrane permeability. Nitrocefin-based colorimetric assay was conducted to assess β-lactamase activity. crystal violet(CV) staining was conducted to assess the effect of CAZ+TRQ on biofilm formation. 2,3-di-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazole-5-anilinoyl(XTT) reduction assay was conducted to assess the effect of CAZ+TRQ on viable bacterial counts within biofilms. These results indicated that TRQ significantly inhibited the efflux pump function of PA(P&lt;0.01), increased outer membrane permeability(P&lt;0.05), reduced β-lactamase activity(P&lt;0.01), and synergizing with CAZ to inhibit early biofilm formation and the viable bacterial counts within biofilms(P&lt;0.01). A clinical study enrolled 20 patients with ARI caused by drug-resistant PA, who were randomly divided into control group(CAZ monotherapy) and experimental group(CAZ combined with TRQ). The sputum culture negative conversion, changes in resistance-related gene expression, inflammatory indicators, and symptom scores were compared between the two groups. The results demonstrated that the experimental group exhibited a higher sputum culture negativity rate, more pronounced downregulation of resistance-related gene expression, greater improvement in inflammatory indicators(P&lt;0.05), and a more substantial reduction in the cough and sputum assessment questionnaire(CASA-Q) scores(P&lt;0.05). In conclusion, this study systematically demonstrated that the combination of CAZ and TRQ can modulate the resistance mechanism of PA through multiple targets, enhance antibacterial efficacy and significantly improve clinical infectious symptoms and inflammatory responses, thereby providing both experimental and clinical evidence for integrated traditional Chinese and western medicine to combat bacterial resistance.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 18","pages":"5397-5407"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Effects of Shufeng Jiedu Capsules on lung injury repair and T cell subset proportions during recovery period in mice with influenza A H1N1 pneumonia].","authors":"Xin-Ying Li, Lei Bao, Shu-Ran Li, Rong-Hua Zhao, Jing Sun, Dan Xie, Shan-Shan Guo, Xiao-Lan Cui, Zi-Han Geng","doi":"10.19540/j.cnki.cjcmm.20260523.801","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260523.801","url":null,"abstract":"<p><p>This study investigated the effects of Shufeng Jiedu Capsules(SFJD) on pharmacodynamics, T helper cell(Th) proportions, and CD8~+T-cell immune memory formation during the recovery phase in mice infected with influenza A H1N1 virus. A non-lethal pneumonia mouse model was established by intranasal inoculation with influenza A virus A/PR/8/34(PR8) strain. Mice were randomly divided into three time-point groups: 7, 10, and 13 days post-infection(dpi), with 30 mice in each group. At each time point, mice were further randomly divided into a normal group, PR8 model group, positive drug group(oseltamivir phosphate, 0.027 5 g·kg~(-1)·d~(-1)), and high-and low-dose SFJD groups(2.558 and 1.279 g·kg~(-1)·d~(-1)), with six mice in each subgroup. From 0 dpi until the day of sample collection(7, 10, or 13 dpi), mice were administered the corresponding drugs by gavage, while the normal and PR8 model groups received equal volumes of deionized water. At the indicated time points, mice were sacrificed for sample collection. Lung and body weights were measured to calculate the lung index. At 10 dpi, Micro-CT was used to observe lung imaging changes. Viral load in lung tissue was detected by qRT-PCR. Flow cytometry was used to determine the proportions of CD4~+T cells and CD8~+T cells in peripheral blood and lung tissue at the three time points. Based on preliminary experimental results, 10 dpi was selected for further analysis of T-cell subsets in lung tissue by flow cytometry, including Th1 and Th2, as well as naive CD8~+T cells, central memory CD8~+T cells, effector CD8~+T cells, and memory precursor effector CD8~+T cells. The results showed that SFJD increased body weight and reduced lung index at all three time points, improved lung morphology at 10 dpi, and reduced viral load in lung tissue. SFJD also increased the proportion of CD8~+T cells in peripheral blood at 7 dpi, increased the proportion of CD4~+T cells in lung tissue at 7 dpi, and reduced the proportion of CD8~+T cells in lung tissue at 7, 10, and 13 dpi. Based on analyses of lung index and the proportions of CD4~+ and CD8~+T cells in peripheral blood and lung tissue at the three time points, 10 dpi was selected to investigate the effects of SFJD on T-cell subsets in lung tissue. SFJD promoted recovery from mild influenza A H1N1 viral pneumonia by inhibiting differentiation of Th1 cells and effector CD8~+T cells, while promoting the generation of naive CD8~+T cells, central memory CD8~+T cells, and memory precursor effector CD8~+T cells, thereby preventing persistent inflammation and facilitating immune memory formation.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 18","pages":"5198-5207"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Effects of gambogic acid on liver function in rats with chronic hepatitis B by adjusting Sirt1/FoxO1 pathway].","authors":"Xing Ouyang, Min Liu, Xin Hu","doi":"10.19540/j.cnki.cjcmm.20260519.801","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260519.801","url":null,"abstract":"<p><p>This study investigated the effects of gambogic acid(GA) on liver function in rats with chronic hepatitis B(CHB) via the silent information regulator 2 homolog 1(Sirt1)/forkhead box transcription factor O1(FoxO1) signaling pathway. A CHB rat model was established using hepatitis B virus(HBV) antigen. Another 10 healthy rats injected with an equal volume of physiological saline served as the control group. After successful modeling, rats were divided into a CHB group, low-dose GA(L-GA, 50 mg·kg~(-1) GA by gavage) group, high-dose GA(H-GA, 100 mg·kg~(-1) GA by gavage) group, and GA+EX527(100 mg·kg~(-1) GA by gavage combined with intraperitoneal injection of 5 mg·kg~(-1) EX527, a Sirt1 inhibitor) group. Rats in the control and CHB groups received equal volumes of physiological saline by gavage and intraperitoneal injection. Each group consisted of 10 rats, and treatment was administered once daily for 4 consecutive weeks. Serum levels of aspartate aminotransferase(AST), alanine aminotransferase(ALT), and total bilirubin(TBIL) were measured using an automated biochemical analyzer. ELISA was performed to determine the serum levels of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α). RT-qPCR was used to detect viral expression in liver tissue. HE staining was performed to observe pathological changes in liver tissue, and Masson staining was used to evaluate hepatic fibrosis. Western blot was used to detect the protein expression of Sirt1 and acetylated(Ac)-FoxO1/Fox O1 in liver tissue. The results showed that liver tissue in the CHB group exhibited marked swelling, disordered cellular arrangement, extensive inflammatory cell infiltration, and collagen deposition. Treatment with L-GA and H-GA progressively alleviated pathological injury and collagen deposition in liver tissue, whereas pathological injury and collagen deposition were further aggravated in the GA+EX527 group. Compared with the control group, the CHB group showed significantly increased levels of ALT, AST, TBIL, IL-1β, TNF-α, and HBV DNA, and significantly decreased expression of Sirt1 and Ac-FoxO1/Fox O1(P&lt;0. 05). Compared with the CHB group, the L-GA and H-GA groups showed significantly decreased levels of ALT, AST, TBIL, IL-1β, TNF-α, and HBV DNA, and significantly increased expression of Sirt1 and Ac-FoxO1/Fox O1(P&lt;0. 05), with more pronounced changes observed in the H-GA group(P&lt;0. 05). Treatment with GA+EX527 significantly reversed the changes in the above indicators observed in the H-GA group(P&lt;0. 05). In conclusion, GA may improve liver function in CHB rats by activating the Sirt1/Fox O1 signaling pathway, thereby inhibiting inflammatory responses and hepatic fibrosis and reducing viral expression in liver tissue.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 17","pages":"5003-5008"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149185122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Effects and mechanisms of Supplemented Shenqi Dihuang Decoction Formula improving renal aging and tubulointerstitial fibrosis in diabetic kidney disease by inhibiting ferroptosis].","authors":"Ya-Jing Li, Dong-Wei Cao, Wei Wu, Yi-Gang Wan, Hao-Wen Shen, Qi-Han He, Tian-Qing Sang, Ying-Lu Liu, Qi-Jun Fang, Yue Tu, Fee-Lan Chong","doi":"10.19540/j.cnki.cjcmm.20260317.701","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260317.701","url":null,"abstract":"&lt;p&gt;&lt;p&gt;This study aimed to explore the effects and mechanisms of Supplemented Shenqi Dihuang Decoction Formula(SSDDF) in ameliorating renal aging(RA) and tubulointerstitial fibrosis(TIF) in diabetic kidney disease(DKD) by inhibiting ferroptosis, in comparison with empagliflozin(EMPA), a novel hypoglycemic agent. For the in vivo experiment, a type 2 DKD rat model with histopathological characteristics of RA and TIF was established. After successful modeling, the model rats were divided into the low-dose SSDDF(SSDDF-L) group, high-dose SSDDF(SSDDF-H) group, EMPA group and normal saline control group, and were administrated by gavage for six consecutive weeks for intervention. For the in vitro experiment, a senescent model of renal tubular epithelial cells was constructed by treating NRK-52E cells with high glucose(HG), which was then intervened with SSDDF-L containing serum, SSDDF-H containing serum, EMPA, as well as ferroptosis and iron metabolism inhibitors. In both in vivo and in vitro studies, aging phenotypes and related physiological indicators including body weight(BW) and blood glucose(BG), renal injury indicators including serum creatinine(Scr), blood urea nitrogen(BUN) and urinary N-acetyl-β-D-glucosaminidase(UNAG), aging characteristics of renal tissues and cells including senescence-associated β-galactosidase(SA-β-gal) staining and protein expression of klotho and p16, TIF pathological features and cellular fibrotic injury, senescence-associated secretory phenotype(SASP), and ferroptosis characteristics(lipid peroxidation-dependent ferroptosis detected by Ferro Orange fluorescent probe and mitochondrial transmission electron microscopy) were examined and compared. Meanwhile, an &quot;SSDDF-component-target&quot; network was constructed via network pharmacology, and Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses were combined to screen the core signaling pathways. Non-targeted metabolomics was adopted to analyze the characteristics of renal tissues, screen potential biomarkers and enrich related metabolic pathways.The results indicated that the effect of SSDDF in ameliorating RA and TIF in DKD rats might be associated with the regulation of ferroptosis signaling pathways. In the in vivo experiment, SSDDF ameliorated the aging phenotypes, BW, BG, UNAG levels, as well as RA and TIF in DKD model rats, with SSDDF-H exerting a superior effect to SSDDF-L; notably, SSDDF-H showed a better effect than EMPA in improving Scr and BUN levels. SSDDF also ameliorated renal lipid peroxidation-dependent ferroptosis in DKD rats, where SSDDF-H had a better effect than SSDDF-L and an equivalent effect to EMPA. In the in vitro experiment, SSDDF-H containing serum multi-targetedly improved HG-induced senescence, fibrotic injury, SASP expression, ferroptosis marker levels and mitochondrial ultrastructural damage in renal tubular epithelial cells, with its effect comparable to that of ferroptosis or iron metaboli","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 18","pages":"5131-5145"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149185928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Mechanism of gypenoside LI inducing apoptosis and autophagy in clear cell renal cell carcinoma cells via ROS/JNK and Akt/mTOR signaling pathways].","authors":"An-Xin Wang, Yu-Jie Wei, Ru-Yi Liu, Qi Huang, Hao Yu, Xiu-Ming Li, Hui Liu","doi":"10.19540/j.cnki.cjcmm.20260601.705","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260601.705","url":null,"abstract":"<p><p>This study aims to investigate the anti-proliferative effect and molecular mechanism of gypenoside LI(Gyp LI) in clear cell renal cell carcinoma(ccRCC) and elucidate its regulatory effect on apoptosis, autophagy, reactive oxygen species(ROS) signals, and related pathways. The effect of Gyp LI on ccRCC cell viability, proliferation, apoptosis, autophagy, and migratory capability was observed and assessed by cell counting kit-8(CCK-8), colony formation test, flow cytometry, Hoechst staining, wound healing assay, and transmission electron microscope(TEM). RNA sequencing, gene set enrichment analysis(GSEA), and Western blot were used to identify and verify the signaling pathways involved. The results show that Gyp LI significantly inhibits the proliferation of ACHN cells and 769-P cells, with IC_(50) values of 72. 30 and 62. 57 μmol·L~(-1) after treatment for 48 hours. Meanwhile, Gyp LI induced nuclear pyknosis and karyorrhexis, inhibited colony formation and cell migration, upregulated the expressions of B-cell lymphoma-2 associated X protein(Bax), cysteinyl aspartate-specific proteinase-3(caspase-3), microtubule-associated protein 1A/1B-light chain 3(LC3)-Ⅱ/LC3-Ⅰ, autophagy-related protein 5( ATG5), phosphorylated c-Jun n-terminal kinase( p-JNK), and phosphorylated p38 mitogen-activated protein kinase( p-p38 MAPK), downregulating the expressions of B-cell lymphoma-2( Bcl-2), sequestosome 1(p62), phosphorylated protein kinase B(p-Akt), and phosphorylated mammalian target of rapamycin(p-mTOR). Mechanistically, Gyp LI activated c-Jun N-terminal kinase( JNK)/p38 mitogen-activated protein kinase( p38 MAPK) pathways, inhibited protein kinase B(Akt)/mammalian target of rapamycin(mTOR) pathways, and promoted autophagy in ccRCC cells. Autophagy inhibition further enhanced apoptosis. Gyp LI also markedly induced ROS production, and this effect was partially reversed by N-acetyl-Lcysteine(NAC). Subcutaneous xenograft experiments of ACHN cells in BALB/c nude mice demonstrate that gypenosides can safely and effectively inhibit tumor growth. In conclusion, Gyp LI exerts anti-ccRCC effects by coordinately regulating ROS-mediated stress signaling, mitochondrial apoptosis, and autophagy.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 17","pages":"5040-5052"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149185939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Visual analysis of research status and frontier trend of Panlongqi Tablets].","authors":"Jia-Lin Wang, Xiao-Xuan Li, Qian-Qian Yan, Qing-Yu Zhao, Li-Ting Xu, Li-Li Wang, Teng-Fei Han, Chun-Fang Liu, Na Lin","doi":"10.19540/j.cnki.cjcmm.20250320.401","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20250320.401","url":null,"abstract":"<p><p>Through bibliometrics and CiteSpace visualization software, this study explored the hot spots and directions of research on the Chinese medicine compound Panlongqi Tablets, providing directions for related research. The databases of CNKI, Wanfang, VIP, Sino Med, and Web of Science were searched. CiteSpace 6. 3 R1 software was used for visual analysis of the relevant literature on Panlongqi Tablets from the establishment of these databases to January 8, 2025. Finally, 160 pieces of literature on Panlongqi Tablets were included, mainly clinical papers. Panlongqi Tablets were recommended by nine guidelines and had six invention patents. There are multiple publishing teams and institutions, with the team of ZHANG De-zhu and LIN Na having the largest number of publications(five papers each). Shaanxi Panlong Pharmaceutical Group Limited by Share LTD. and China Academy of Chinese Medical Sciences are the main publishing institutions, and there is less cooperation between different authors and institutions. In terms of keyword analysis, the main keywords are &quot; controlled study&quot; &quot; fracture&quot; &quot; rheumatoid arthritis&quot; &quot; osteoarthritis&quot; &quot; Meta-analysis&quot; &quot; network pharmacology&quot;, and so on. A total of 19 clusters were obtained, which were grouped into four cluster themes: clinical research, pharmacological experiments, chemical components, and safe drug use. The current focus is mainly on the evaluation of clinical efficacy and pharmacological effects of osteoarthritis, fracture, and other orthopedic diseases, the determination of effective components of Panlongqi Tablets, and drug safety. Future research can combine multidisciplinary technology and artificial intelligence to fully explore the clinical characteristics and advantages of the &quot; Qi yao&quot; represented by Panlongqi Tablets, expand the indications, and complete a clearer definition of safety.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 17","pages":"4817-4826"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149185960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Mechanism of action of steamed Polygonati Rhizoma in ameliorating pulmonary fibrosis in mice based on PI3K/AKT signaling pathway].","authors":"Min Shen, Jing-Jing Chen, Xun Liu, Yang Zhou, Jie Cao, Xin Li, Kui-Long Wang, Hong-Li Yu","doi":"10.19540/j.cnki.cjcmm.20260629.301","DOIUrl":"https://doi.org/10.19540/j.cnki.cjcmm.20260629.301","url":null,"abstract":"<p><p>This paper aims to investigate the therapeutic effect and mechanism of steamed Polygonati Rhizoma on pulmonary fibrosis in mice. A mouse model of pulmonary fibrosis was established and treated with steamed Polygonati Rhizoma water decoction by gavage. Therapeutic efficacy was evaluated through histopathological observation of lung tissue, assessment of fibrosis severity, determination of lung hydroxyproline(HYP) content, and measurement of inflammatory cytokines(IL-1β and TNF-α) in bronchoalveolar lavage fluid. The targets of active components in steamed Polygonati Rhizoma were predicted using the Swiss Target Prediction database. Disease-related targets of pulmonary fibrosis were obtained from the GeneCard and OMIM databases, followed by intersection analysis with the targets of active components using the Venny 2.1.0 platform. The target network and protein-protein interaction(PPI) network were constructed. Key pathways were screened through KEGG pathway enrichment analysis. The expression levels of collagen Ⅰ, fibronectin, phosphorylated AKT(p-AKT), and phosphorylated PI3K(p-PI3K) proteins in lung tissue were detected by immunofluorescence and Western blot. RESULTS:: show that a total of 12 active components and 319 predicted targets were screened from Polygonati Rhizoma. After intersecting with 6 308 pulmonary fibrosis-related targets, 245 common targets were obtained. KEGG enrichment analysis identified the PI3K/AKT signaling pathway as the core pathway. In vivo experiments confirmed that steamed Polygonati Rhizoma significantly alleviated pathological damage in the lung tissue, reduced HYP content, suppressed inflammatory cytokine levels, and down-regulated the expression levels of collagen Ⅰ and fibronectin. Flavonoid components, such as 4',5-dihydroxyflavone and baicalein, were speculated to be potentially associated with these therapeutic effects. These findings indicate that steamed Polygonati Rhizoma exerts anti-pulmonary fibrosis effects by regulating the PI3K/AKT signaling pathway via its active flavonoid components, thereby ameliorating pulmonary inflammation and collagen deposition.</p>","PeriodicalId":52437,"journal":{"name":"Zhongguo Zhongyao Zazhi","volume":"51 18","pages":"5273-5281"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149186024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}