{"title":"Morroniside Inhibits apoptosis and Oxidative Stress in High Glucose-Induced Renal Tubular Epithelial Cells by Upregulating MiR-25","authors":"Wei Wei, Huimin Wang, Byung Pal Yu","doi":"10.32383/appdr/202126","DOIUrl":"https://doi.org/10.32383/appdr/202126","url":null,"abstract":"Objective: Morroniside has been shown to have anti-apoptotic and anti-oxidative stress effects, but its role in diabetic nephropathy (DN)-related cell injury is still unclear. This study aims to explore the role and mechanism of morroniside in DN progression. Methods: Human renal tubular epithelial cells (HK2) were cultured with high glucose (HG) and treated with morroniside. Cell proliferation and apoptosis were measured by cell counting kit 8 method and flow cytometry. Western blot was used to detect the protein levels of apoptosis marker Bax and anti-apoptosis marker Bcl-2. Malonaldehyde (MDA) and superoxide dismutase (SOD) levels were examined to evaluate cell oxidative stress, and miR-25 expression was determined by quantitative real-time PCR. Results: After treated with HG, cell viability, Bcl-2 level, SOD activity and miR-25 expression were decreased, whereas apoptosis rate, Bax level and MDA content were increased. Morroniside enhanced cell viability, Bcl-2 level, SOD activity and miR-25 expression, while reduced apoptosis rate, Bax level and MDA content in HG-induced HK2 cells. Overexpression of miR-25 promoted cell viability, repressed HG-induced HK2 cell apoptosis and oxidative stress. Knockdown of miR-25 reversed the effects of morroniside on the viability, apoptosis and oxidative stress in HG-induced HK2 cells. Conclusion: Morroniside could inhibit HG-induced HK2 cell injury via increasing miR-25 expression, confirming that morroniside might alleviate DN process.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 6","pages":"1013-1020"},"PeriodicalIF":0.0,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/202126","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147896095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Therapeutic Effect and Mechanism of Cardamonin on Periodontitis Rats via Nrf2/HO-1/NLRP3 Signaling Pathway Regulation","authors":"Wenge Lu, Jing An, Jingjing Wang","doi":"10.32383/appdr/197269","DOIUrl":"https://doi.org/10.32383/appdr/197269","url":null,"abstract":"Abstract: This study investigates the therapeutic effects of cardamonin on periodontitis rats and its involvement in the Nrf2/HO-1/NLRP3 signaling pathway. Fifty SD rats were divided into five groups: CON, MOD, L-CAR (15 mg/kg), H-CAR (60 mg/kg), and H-CAR+BRU (60 mg/kg + 2 mg/kg). ELISA was used to measure serum inflammatory and oxidative stress factors. Micro-CT assessed alveolar bone absorption, and HE staining evaluated periodontal tissue. TRAP staining was performed for osteoclast counting, and Western blot measured protein expression of OPG, RANKL, Nrf2, HO-1, and NLRP3. Results showed that, compared to the CON group, rats in the MOD group exhibited gingival erosion, widened periodontal ligament space, and increased inflammatory infiltration, along with reduced alveolar bone parameters (Tb.N, Tb.Th) and lower serum antioxidant levels (SOD, GSH-Px). In contrast, the L-CAR and H-CAR groups showed improved tissue morphology, increased alveolar bone parameters, and enhanced antioxidant levels. These groups also exhibited upregulation of Nrf2 and HO-1 and downregulation of NLRP3, RANKL, and osteoclast count. However, the H-CAR+BRU group showed exacerbated periodontal damage and further imbalance in inflammatory and bone resorption markers. In conclusion, cardamonin exerts therapeutic effects on periodontitis by activating the Nrf2/HO-1 pathway and inhibiting NLRP3-mediated inflammation and bone resorption.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 5","pages":"869-877"},"PeriodicalIF":0.0,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/197269","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ya-yun Chen, Qing Zhu, Xiao-li Zhu, H Li, F. J. Li
{"title":"Study on Chemical Constituents and Cytotoxicity of Scutellaria barbata D. Don Oil Against SMMC-7721","authors":"Ya-yun Chen, Qing Zhu, Xiao-li Zhu, H Li, F. J. Li","doi":"10.32383/appdr/196240","DOIUrl":"https://doi.org/10.32383/appdr/196240","url":null,"abstract":"The anti-neoplastic activities of Scutellaria barbata D. Don have been extensively studied for many years. To investigate the constituents and cytotoxicity of fatty oils extracted from different parts of Scutellaria barbata D. Don, namely seeds, stems, leaves, roots, and flowers, the oils were derived and analyzed using GC-MS. The anti-hepatoma activities of these fatty oils against the SMMC-7721 cell line were evaluated through cell viability assay, Hoechst 33258 staining, and V-FITC/PI staining assay. Western blot analysis quantified apoptosis-related proteins in SMMC-7721 cells treated with SBO. The results demonstrated that SBO exhibited significant anti-hepatoma activities. Fluorescent microscope analysis revealed nucleus shrinkage or fragmentation in cells incubated with SBO, while flow cytometry confirmed pro-apoptotic effects. Protein analysis indicated that SBO induced apoptosis by down-regulating Bcl-2 and p-STAT3, up-regulating Bax, as well as activating caspase 9, caspase 8, and caspase 3 cleavage. The potential mechanisms of SBO-induced apoptosis involved the caspase-8/caspase-3 pathway, the Bcl-2/bax/caspase-9/caspase-3 pathway, and the IL-6/STAT3 pathway.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 5","pages":"831-839"},"PeriodicalIF":0.0,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/196240","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147908086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Guangying Tang, Weiqiang Wu, Pushan Xiao, Zhiliu Tang, G. X. Wang
{"title":"Anti-Inflammatory and Antiarthritic Activity of Procaine-1,3,5-Triazine Derivative for Possible Benefit in Rheumatoid Arthritis: An In Vivo Study","authors":"Guangying Tang, Weiqiang Wu, Pushan Xiao, Zhiliu Tang, G. X. Wang","doi":"10.32383/appdr/197312","DOIUrl":"https://doi.org/10.32383/appdr/197312","url":null,"abstract":"The present study aimed to evaluate the pharmacological effects of a procaine-1,3,5-triazine (PT) derivative on Complete Freund’s Adjuvant (CFA)-induced arthritis in rats. The PT compound was synthesized with excellent yield and purity using a straightforward nucleophillic synthetic approach via reacting procaine with di-substituted 1,3,5-triazine derivative. Arthritis was induced using CFA, and the PT derivative was administered at varying doses (5, 10, and 15 mg/kg.body weight). Throughout the study, multiple physical and biochemical parameters were assessed to determine the therapeutic impact. PT treatment significantly reduced paw swelling and improved body weight in a dose-dependent manner. Biochemical analysis revealed a marked decrease in pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-17) along with an upregulation of anti-inflammatory cytokines (IL-10, IL-4), indicating a potent anti-inflammatory response. Additionally, PT restored oxidative stress markers—such as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH)—to levels close to those in healthy controls. In summary, these findings demonstrate that the procaine-1,3,5-triazine derivative offers significant pharmacological benefits by alleviating CFA-induced rheumatoid arthritis through anti-inflammatory, and antioxidant actions.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 5","pages":"785-791"},"PeriodicalIF":0.0,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/197312","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147885755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhenxing Xu, Tingting Yuan, Lihong Tong, Zhanyong Shao, Lianglong Wang
{"title":"CANTHARIDIN INHIBITS COLON CANCER THROUGH miR-192-5p UPREGULATION","authors":"Zhenxing Xu, Tingting Yuan, Lihong Tong, Zhanyong Shao, Lianglong Wang","doi":"10.32383/appdr/193245","DOIUrl":"https://doi.org/10.32383/appdr/193245","url":null,"abstract":"Abstract: Colon cancer (CC) is a serious threat to human health. Cantharidin (CTD) has anti-cancer properties. This study aims to explore the mechanism of CTD in treating CC. We used CCK-8, Transwell, and Annexin V/PI double staining analyses to detect the effects of CTD on the proliferation, migration, invasion, and apoptosis of CC cells. The effect of CTD on tumor growth was investigated by constructing a CC mouse model. Wild-type or mutant WNK1 luciferase vectors were constructed to verify the interaction between miR-192-5p and WNK1 mRNA. In the CTD group: miR-192-5p level was elevated and the OD values at 450 nm were significantly decreased; the quantity of CC cells passing the Transwell chamber (without or with matrigel) was reduced; the number of apoptotic cells increased obviously; the volume and weight of tumor decreased significantly. These results were reversed by miR-192-5p inhibitor. In HT-29 cells transfected with the wild-type WNK1 vector, the luciferase activity decreased with the miR-192-5p mimic but increased with the miR-192-5p inhibitor. The inhibitor of miR-192-5p counteracted the suppression of CTD on WNK1 expression. In summary, we demonstrated that CTD inhibited CC development by up-regulating miR-192-5p targeting WNK1, which will provide a theoretical basis for the application of CTD in the CC treatment.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 4","pages":"619-627"},"PeriodicalIF":0.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/193245","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147907575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Salvianolic acid for injection protected cerebral ischemia/reperfusion injury by autophagy regulation via PI3K/AKT/mTOR pathway in rats","authors":"Yuan Jing, Xiangbo Gou, Congxin Li, Wan Meixu","doi":"10.32383/appdr/195874","DOIUrl":"https://doi.org/10.32383/appdr/195874","url":null,"abstract":"In clinical, Salvianolic Acid for Injection (SAFI) is a traditional compound preparation used to treat cerebral ischemia/reperfusion (I/R). We aimed to research protective effect and mechanism of SAFI on cerebral I/R. The middle cerebral artery occlusion/reperfusion (MCAO/R) rats and oxygen-glucose deprivation/reperfusion (OGD/R) cell were used in this research. After treated with SAFI and DL-3-n-butylphthalide (NBP), modified neurological severity score (mNSS), histopathology, regional cerebral blood flow (rCBF), cerebral infarction size and the brain water content of rats were measured. Meanwhile, superoxide dismutase (SOD), the interleukine 1-beta (IL-1β), thromboxane B2 (TXB2), malondialdehyde (MDA), 6-keto-PGF1α and brain-derived neurotrophic factor (BDNF), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) of I/R tissue were measured by the ELISA kits. For the experiment in vitro, the cell viability, LC3II, beclin-1 and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mTOR protein levels were confirmed by western blot. The results illustrated SAFI decreased the mNSS, cerebral infarct size, brain water content, IL-1β, TXB2, MDA, IL-6 and TNF-α levels of I/R rats obviously. SAFI also up-regulated the rCBF, 6-keto-PGF1α, BDNF and SOD levels of I/R rats. The in vitro experiments showed that SAFI could promote the PC12 cell proliferation. The down-regulated LC3II and beclin-1 expression in the SAFI treated cells showed that SAFI could proper regulate autophagy for the PC12 cells in OGD/R group. Finally, the autophagy inhibition caused by SAFI on OGD/R cells were reversed by LY294002 and rapamycin (RAPA). These results suggested the PI3K/AKT/mTOR activation played an essential role on the autophagy regulation caused by SAFI.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 4","pages":"715-727"},"PeriodicalIF":0.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/195874","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147893208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
An-lu Shen, Yong-qin Du, Min Ye, Lan Zhou, Hui-min Ding, Zi-qing Hu, Peng Zhou
{"title":"Kaempferol Protects Against Streptozotocin-Induced Diabetic Cardiomyopathy in Rats by Inhibition of the NLRP3/Caspase-1 Signaling Pathway","authors":"An-lu Shen, Yong-qin Du, Min Ye, Lan Zhou, Hui-min Ding, Zi-qing Hu, Peng Zhou","doi":"10.32383/appdr/194778","DOIUrl":"https://doi.org/10.32383/appdr/194778","url":null,"abstract":"Kaempferol (KPF) attenuates diabetic cardiomyopathy (DCM) in streptozotocin (STZ)-treated rats through its hypoglycaemic and insulin-releasing effects, however, the mechanism of KPF protects against DCM is unclear. This study was to reveal the cardioprotective mechanism of KPF. Molecular docking was used to predict the target of KPF. STZ-induced diabetes mellitus (DM) rats was established. The model rats with successful modeling were randomly divided into DM group, KPF group (10 mg/kg), and metformin (Met) group (120 mg/kg). The CTL group and DM group were gavaged with equal amounts of CMC-Na, and all groups were intervened for eight weeks. The changes of blood glucose in different groups was detected. Hematoxylin-eosin (HE), and Masson staining were used to assess pathological changes. Creatine kinase (CK), and B-type natriuretic peptides (BNP) levels were examined. RT-qPCR was used to detect the mRNA expression levels of toll-like receptor 4 (TLR4), NOD-like receptor protein 3 (NLRP3), cysteinyl aspartate specific proteinase-1 (Caspase-1), and GSDMD-N-terminal domain (GSDMD-N), and Western blot was used to detect the expression of NLRP3, and GSDMD-N. KPF has a good binding affinity with TLR4. KPF could significantly improve the abnormal elevation of blood glucose, mitigate pathological changes, and reduce CK and BNP levels. Further mechanistic studies found that KPF reduced the mRNA expressions of TLR4, NLRP3, Caspase-1, and GSDMD-N, and decreased the protein expressions of NLRP3, and GSDMD-N. In conclusion, the mechanism of KPF protects against DCM is related to the inhibition of the NLRP3/Caspase-1 signaling pathway, providing a novel mechanism for KPF intervention in DCM.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 4","pages":"685-694"},"PeriodicalIF":0.0,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/194778","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147878312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ChunYong Yang, ZhiQiang Zhou, J Tian, R. Jin, ZhanYong Li
{"title":"Inhibition of Colon Cancer Xenograft Growth by Celecoxib Analog OSU-03013 Through Wnt/β-Catenin Pathway Modulation","authors":"ChunYong Yang, ZhiQiang Zhou, J Tian, R. Jin, ZhanYong Li","doi":"10.32383/appdr/191339","DOIUrl":"https://doi.org/10.32383/appdr/191339","url":null,"abstract":"OSU-03013 is a Celecoxib analog that dose not inhibit COX-2 expression. OSU-03013 effectively mimics the anti-tumor effects of Celecoxib, however, its exact mechanism in colon cancer (CC) is unknown. SW480 cells were injected subcutaneously into the axilla of nude mice until the volume of the transplanted tumor reached 80 mm3. SW480 cells were inoculated into the tail vein of nude mice to establish a liver metastasis model of CC. OSU-03013 was administered by gavage. The pathology of the tumor tissues was assessed using HE staining and cell apoptosis was measured using TUNEL staining. EMT markers in the tumors were determined using Western Blot, and IL-1β and TNF-α were determined using ELISA. VEGF-A and VEGFR-2 in tumor tissues were measured to assess angiogenesis using immunofluorescence. HE staining was conducted to detect the effect of OSU-03013 on liver metastasis. Western Blot assay was performed to determine the expression of Wnt2, β-catenin and GSK-3β. OSU-03013 reduced inflammatory cell infiltration and inhibited IL-1β and TNF-α production by modulating the Wnt/β-catenin pathway. OSU-03013 induced apoptosis of cancer cells in tumor tissues and possessed anti-angiogenic activity. OSU-03013 treatment reduced the number and size of metastatic nodules of cancer cells in liver tissues. OSU-03013 may inhibit tumor growth and angiogenesis through the Wnt3a/β-catenin pathway in CC nude mice.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 3","pages":"385-398"},"PeriodicalIF":0.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/191339","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147914084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Anticancer effects of emetine against cisplatin resistant pancreatic cancer cells via activation of Cyto-c/Caspase-9/Caspase-3/Bax/Bad axis","authors":"Ting Yin, Yin Zhao, Hui Yang","doi":"10.32383/appdr/190457","DOIUrl":"https://doi.org/10.32383/appdr/190457","url":null,"abstract":"This investigation examines the potential pharmacotherapeutic efficacy of emetine, a natural alkaloid, against pancreatic ductal carcinoma, utilizing the PaCa3 cell line as a model. Employing a multifaceted approach, the study explores emetine's impact on cell viability, clonogenic potential, and apoptotic pathways, unravelling its molecular mechanisms. Additionally, an in-vivo assessment is conducted to evaluate emetine's antitumor efficacy against PaCa3 xenografts. Under standard conditions, PaCa3 cells were treated with varying emetine concentrations and subjected to MTT, clonogenic, DAPI, AO/EB, Annexin V-FITC/PI, and Western blot assays. In-vivo experiments involved the administration of emetine to female nude mice with PaCa3 xenografts, with subsequent measurement of tumor weight and volume. Statistical analyses included Tukey-test and ANOVA. Emetine demonstrated a significant and dose- and time-dependent cytotoxic effect on PaCa3 cells, reducing viability from 98% to 8% (***p<0.001). Clonogenic assay indicated a substantial inhibition of colony formation. DAPI staining revealed nuclear chromatin condensation, while AO/EB staining indicated heightened apoptosis. Annexin V-FITC/PI assay exhibited a dose-dependent decrease in normal cell viability and an increase in apoptotic events. Western blot analysis showcased concentration-dependent downregulation of anti-apoptotic Bcl-2 and upregulation of pro-apoptotic markers. In-vivo experiments illustrated a dose-dependent reduction in tumor weight (5 g to 1.6 g) and volume (2400 mm³ to 844 mm³) with emetine treatment. In conclusion, emetine emerges as a potent anticancer agent against pancreatic ductal carcinoma, exhibiting cytotoxicity, clonogenic inhibition, and apoptotic induction in PaCa3 cells. The in-vivo study further highlights its promising therapeutic potential, laying the groundwork for future clinical studies in pancreatic cancer treatment.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 3","pages":"373-384"},"PeriodicalIF":0.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://doi.org/10.32383/appdr/190457","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147898469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
An-lu Shen, Yong-Qin Du, Huimin Ding, Lan Zhou, Youg-Qin Du, Min Ye, Gang Yin
{"title":"Study on the Mechanism of Kaempferol Against Diabetic Nephropathy via NLRP3/Caspase-1 Signaling Pathway","authors":"An-lu Shen, Yong-Qin Du, Huimin Ding, Lan Zhou, Youg-Qin Du, Min Ye, Gang Yin","doi":"10.32383/appdr/192024","DOIUrl":"https://doi.org/10.32383/appdr/192024","url":null,"abstract":"To systematically evaluate the protective effect of kaempferol (KPF) against renal injury in diabetic rats, and to explore the mechanism of KPF via the NLRP3/Caspase-1 signaling pathway. A diabetic rat model was established by high-fat diet combined with STZ induction, and the urinary levels of urinary creatinine, urinary protein and urea nitrogen were detected. HE and Masson staining were used to assess pathological changes. Western blot was used to detect the expression of NLRP3, Cleaved-Caspase1, GSDMD, and GSDMD-N, and RT-qPCR was used to detect the mRNA expression levels of NLRP3, Caspase1, and GSDMD. KPF significantly improved renal function, attenuated pathological changes, and reduced the levels of NLRP3, Cleaved-caspase1, GSDMD, and GSDMD-N protein and mRNA expressions in diabetic nephropathy (DN) rats. KPF has a protective effect against kidney injury in diabetic rats, and its mechanism may be related to the inhibition of the NLRP3/Caspase-1 signaling pathway.","PeriodicalId":7135,"journal":{"name":"Acta Poloniae Pharmaceutica - Drug Research","volume":"81 3","pages":"523-532"},"PeriodicalIF":0.0,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"http://dx.doi.org/10.32383/appdr/192024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147877917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}