Phytomedicine最新文献

{"title":"Shaoyao-Gancao Decoction, a famous Chinese medicine formula, protects against APAP-induced liver injury by promoting autophagy/mitophagy","authors":"","doi":"10.1016/j.phymed.2024.156053","DOIUrl":"10.1016/j.phymed.2024.156053","url":null,"abstract":"<div><h3>Background</h3><div>Acetaminophen (APAP)-induced hepatotoxicity is a major cause of acute liver failure (ALF), during which autophagy is triggered as a cellular defense mechanism. Shaoyao-Gancao Decoction (SGD), a traditional prescription in Chinese Medicine, is renowned for its therapeutic effects on liver diseases. However, the efficacy and mechanisms of SGD in treating APAP-induced liver injury remain underexplored.</div></div><div><h3>Purpose</h3><div>This study aims to provide robust evidence regarding the protective effects of SGD against APAP overdose in vitro and in vivo, as well as to elucidate its hepatoprotective mechanisms and active components.</div></div><div><h3>Study design</h3><div>The hepatoprotective mechanisms and active components of SGD were investigated through a combination of in vivo and in vitro experiments.</div></div><div><h3>Methods</h3><div>The protective effects of SGD on APAP-induced liver injury were assessed using a murine model and primary hepatocytes. RNA sequencing and subsequent experimental validations were conducted to uncover the underlying mechanisms of SGD's hepatoprotective actions. Comprehensive chemical profiling of SGD was performed using UHPLC-Q-Exactive Orbitrap HRMS to identify potential active ingredients. Immunohistochemistry, immunofluorescence, quantitative real-time PCR (qPCR), western blotting, enzyme-linked immunosorbent assay (ELISA), and flow cytometry were utilized to investigate the specific cellular changes in liver tissues and hepatocytes influenced by SGD.</div></div><div><h3>Results</h3><div>SGD was observed to mitigate APAP-induced mitochondrial damage, inflammation, and necrosis by promoting mitochondrial autophagy. The inhibition of autophagy negated the hepatoprotective effects of SGD. Additionally, a detailed characterization of SGD's chemical composition revealed that Licoisoflavone B, Liquiritin, Liquiritin apioside, Licorice saponin G2 and Paeoniflorin Sulfit were potentially critical compounds in the regulation of autophagy and mitophagy.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate that SGD promotes autophagy/mitophagy, which effectively mitigates APAP-induced hepatotoxicity, suggesting SGD's potential as a promising therapeutic agent for APAP-induced liver injury.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142319799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Osmundacetone ameliorates Alzheimer's-like pathologies by inhibiting β-amyloid fibrillation, oxidative damage and neuroinflammation in APP/PS1 transgenic mice","authors":"","doi":"10.1016/j.phymed.2024.156091","DOIUrl":"10.1016/j.phymed.2024.156091","url":null,"abstract":"<div><h3>Background</h3><div>β-Amyloid (Aβ) fibrillation is critical for Aβ deposition and cytotoxicity during the progression of Alzheimer's disease (AD). Consequently, anti-Aβ monoclonal antibody drugs targeting Aβ oligomers and aggregation are considered potential therapeutic strategies for AD treatment. Similar to the working mechanisms of anti-Aβ monoclonal antibody drugs, our study identified <em>osmundacetone</em> (OAC), a small-molecule compound isolated from the traditional Chinese medicine <em>Rhizoma Osmundae</em>, as exerting anti-AD effects by targeting Aβ.</div></div><div><h3>Purpose</h3><div>This study sought to determine whether OAC influences the Aβ burden in APP/PS1 mice and to identify potential regulatory mechanisms.</div></div><div><h3>Methods</h3><div>Five-month-old APP/PS1 mice were injected intraperitoneally with OAC at a dose of 1 mg/kg for 12 weeks. The cognitive functions of the mice were assessed via the Morris water maze test and the open field test. O<em>smundacetone</em> was analyzed via molecular docking, an isothermal dose‒response fingerprint-cellular context thermal shift assay, a thioflavine T fluorescence assay, and an atomic force microscopy assay to analyze the effects of OAC on Aβ fibrillation. Immunofluorescence, immunoblotting, and immunohistochemistry were used to assess Aβ clearance, AD pathology, oxidative stress, and inflammatory responses.</div></div><div><h3>Results</h3><div>The innovative biochemical and physical data illustrated that the ability of OAC to inhibit Aβ fibrillation was accomplished by binding directly to Aβ, which differed from the majority of previously reported natural polyphenols that modulate the Aβ content and structure in an indirect manner. The inhibition of Aβ fibrosis by OAC subsequently promoted Aβ lysosomal degradation, resulting in a decreased Aβ burden in APP/PS1 mice. Furthermore, OAC treatment inhibited oxidative damage by upregulating glutathione peroxidase expression and attenuated the production of inflammatory factors by downregulating nuclear factor-kB phosphorylation in APP/PS1 mice.</div></div><div><h3>Conclusion</h3><div>These findings demonstrate, for the first time, that OAC could reduce the brain Aβ burden in APP/PS1 mice by inhibiting Aβ fibrillation through direct binding to Aβ and improve cognitive dysfunction by attenuating oxidative damage and neuroinflammation. These findings indicate that OAC may be a promising candidate for the treatment of AD.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142324068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics joint analysis reveals that the Miao medicine Yindanxinnaotong formula attenuates non-alcoholic fatty liver disease","authors":"","doi":"10.1016/j.phymed.2024.156026","DOIUrl":"10.1016/j.phymed.2024.156026","url":null,"abstract":"<div><h3>Backgroud</h3><div>Non-alcoholic fatty liver disease (NAFLD) is a growing chronic liver disease worldwide, and no effective agent is approved yet for this condition. Traditional Chinese Medicine (TCM), which has been practiced for thousands of years in China and other Asian countries, is considered an important source for identifying novel medicines for various diseases. Miao medicine Yindanxinnaotong formula (YDX) is a classical TCM for the treatment of hyperlipidemia disease by reducing blood lipid content, while the role of YDX have not been clarified in NAFLD.</div></div><div><h3>Purpose</h3><div>To investigate the protective effect of YDX on NAFLD in mice induced by high fat diet (HFD) and clarify the potential mechanism.</div></div><div><h3>Methods</h3><div>NAFLD mice model was constructed by receiving HFD for 10-week period with or without YDX administration. Lipid profiles, biochemical indicators, and histopathological staining were performed to evaluate the extent of hepatic lipid accumulation and hepatic steatosis. 16<em>S</em> rRNA sequencing was used to determine the gut microbial composition. Serum metabolomics was further used to investigate the changes in plasma biomarkers for NAFLD-associated by UPLC-Q-TOF/MS analysis. Subsequently, liver transcriptomics was employed to identify differentially expressed genes and explore regulatory pathways. Then, lipid metabolism–related proteins and inflammation factors were examined by Western blot and ELISA.</div></div><div><h3>Results</h3><div>YDX reduced body weight gain, liver index and inflammatory cytokines levels, along with improved hepatic steatosis, serum lipid profile, sensitivity to insulin and also tolerance to glucose, and enhanced oxidative defense system in HFD-induced mice. Also, YDX remarkedly affected gut microbiota diversity and community richness and decreased the ratio of <em>Firmicutes/Bacteroidetes</em>. Meanwhile, YDX also reduced the production of harmful lipid metabolites in the sera of NAFLD mice, such as LPC(18:0), LPC(18:1) and carnitine. Notably, consistent with liver transcriptomics results, YDX downregulated the expression of proteins implicated in <em>de novo</em> lipid synthesis (Srebp-1c, Acaca, Fasn, Scd-1, and Cd36) and pro-inflammatory cytokines (IL-6 and TNF-α), and increased the expression of proteins-related fatty acid β-oxidation (Ampkα, Ppar-α, and Cpt-1) in the liver by activating Ampk pathway.</div></div><div><h3>Conclusion</h3><div>YDX is promisingly an effective therapy for preventing NAFLD by modulating the Ampk pathway, inhibiting gut microbiota disorder, and reducing the production of harmful lipid metabolites.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142401058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Araloside A alleviates sepsis-induced acute lung injury via PHD2/HIF-1α in macrophages","authors":"","doi":"10.1016/j.phymed.2024.156089","DOIUrl":"10.1016/j.phymed.2024.156089","url":null,"abstract":"<div><h3>Background</h3><div>Acute lung injury (ALI)-induced acute respiratory syndromes is a critical pathological sequala of sepsis. Araloside A (ARA), extracted from <em>Aralia taibaiensis</em>, possesses anti-oxidative and pro-apoptotic effects, as well as a protective effect against inflammatory diseases such as gastric ulcers. However, its impact on progression of ALI remains unknown. This study seeks to assess the therapeutic effect of ARA in sepsis-induced ALI, and to elucidate the underlying mechanism.</div></div><div><h3>Methods</h3><div>Sepsis-induced ALI was induced in C57BL/6 mice using lipopolysaccharide (LPS) or cecal ligation and puncture (CLP) along with simultaneous administration of ARA. In vitro, bone marrow-derived macrophages (BMDMs) and RAW264.7 cells were exposed to LPS to activate proinflammatory macrophages in the presence/absence of ARA. RNA sequencing of BMDMs was then conducted to elucidate the detailed mechanism.</div></div><div><h3>Results</h3><div>Treatment of mice with ARA led to a significant reduction in serum level of inflammatory cytokines, ameliorated sepsis-induced ALI (i.e., impaired barrier integrity, cell apoptosis), and increased survival of septic mice. <em>In vitro</em>, ARA effectively inhibited activation of proinflammatory BMDMs. In addition, RNA sequencing revealed that the PHD2/HIF-1α signaling played a critical role in the anti-inflammatory effects of ARA. ARA suppressed proinflammatory macrophages to ameliorate lung inflammation in septic mice by restoring PHD2/HIF-1α signaling.</div></div><div><h3>Conclusions</h3><div>ARA prevented mice from the fatal effects of sepsis by restoring PHD2/HIF-1α signaling, thereby inhibiting activation of proinflammatory macrophages. These findings suggest that ARA could be a promising therapy for sepsis-induced ALI.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dioscin improves fatty liver hemorrhagic syndrome by promoting ERα-AMPK mediated mitophagy in laying hens","authors":"","doi":"10.1016/j.phymed.2024.156056","DOIUrl":"10.1016/j.phymed.2024.156056","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Mitochondria play a crucial role in upholding metabolic homeostasis. Mitochondrial damage closely associated with the pathogenesis of fatty liver hemorrhagic syndrome (FLHS), while mitophagy being among the most effective methods for eliminating the damaged mitochondria. Dioscin, a natural extract, can activate autophagy; however, its effects on FLHS regarding mitophagy regulation remain unelucidated.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Purpose&lt;/h3&gt;&lt;div&gt;We explored the impact of dioscin on FLHS induced by a high-energy and low-protein (HELP) diet in laying hens, mainly focused the protective effects of dioscin on mitochondrial injury.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Method&lt;/h3&gt;&lt;div&gt;To investigate the impact of dioscin on fatty liver syndrome in laying hens, we first induced the condition by feeding them a high-energy and low-protein diet. Then, we assessed lipid metabolism-related markers using oil red staining and a commercial detection kit. In addition, the role of dioscin on fatty liver syndrome in laying hens was confirmed by assessing the activation of hepatocyte fat deposition and hepatocyte apoptosis; and the mechanism of dioscin in FLHS was investigated through LMH cell experiment in vitro. Furthermore, CETSA and molecular docking were conducted for additional confirmation.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Result&lt;/h3&gt;&lt;div&gt;The results showed that dioscin alleviated mitochondrial damage, relieved the excessive deposition of hepatic lipid droplets and oxidative stress induced by HELP diet in laying hens. Furthermore, dioscin regulated the mitophagy by activating the estrogen receptor α (ERα)/adenosine 5′-monophosphate-activated protein kinase (AMPK) signaling pathway, thus mitigating mitochondria injury and apoptosis in hepatocytes. In addition, we found that dioscin promoted the translocation of nuclear transcription factor into nucleus by activating ERα-AMPK signaling, facilitating autophagic flux in the liver of laying hens and LMH cells. Furthermore, cells pretreated with the lysosomal acidification inhibitor bafilomycin A1 blocked the inhibitory effect of dioscin on the apoptosis induced by palmitic acid (PA)-stimulation in LMH cells, suggesting that dioscin reduces PA-induced apoptosis by activating mitophagy. Moreover, dioscin-induced lysosomal acidification and mitochondrial biogenesis were reversed in PA-induced LMH cells pretreated with ERα-specific inhibitor methylpiperidino pyrazole.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;This study firstly demonstrated that dioscin alleviates fatty liver syndrome induced by HELP diet in laying hens. The findings from this study illustrated that dioscin plays a significant role in reducing mitochondrial damage and apoptosis, and these beneficial effects mainly achieve through promotion of ERα-AMPK signaling, which mediates autophagy within the liver of laying hens fed a HELP-diets. These findings provide a theoretical basis for considering dioscin as a possible treatment option for mitigating FLHS in egg-la","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142352538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gelsevirine ameliorates sepsis-associated encephalopathy by inhibiting the STING signalling-mediated pyroptosis pathway in microglia","authors":"","doi":"10.1016/j.phymed.2024.156071","DOIUrl":"10.1016/j.phymed.2024.156071","url":null,"abstract":"<div><h3>Background</h3><div>Sepsis-associated encephalopathy (SAE) is among the most prevalent and deadly complications associated with sepsis, but satisfactory treatments and therapeutic agents are lacking. Gelsevirine, an active ingredient derived from <em>Gelsemium elegans</em> Benth., has shown promising effects in animal models of anxiety, ischaemic stroke and osteoarthritis. However, its protective effect against SAE and its mechanism of action are still unknown.</div></div><div><h3>Purpose</h3><div>To elucidate the efficacy of gelsevirine against SAE and the mechanism of its protective effect through the STING signalling-mediated pyroptosis pathway.</div></div><div><h3>Methods</h3><div>We constructed a mouse model of caecum ligation and puncture (CLP)-induced sepsis and explored the protective effects of gelsevirine in mice with SAE by assessing survival rates and behavioural alterations. To further explore its mechanism of action, we investigated the modulatory effects of gelsevirine on the levels of inflammatory factors, microglial activation and pyroptosis by Western blotting, immunohistochemistry staining and PCR. STING knockout mice were used to verify the protective effect of gelsevirine against SAE through the STING pathway.</div></div><div><h3>Results</h3><div>Gelsevirine increased the survival rate of mice with SAE. The Morris water maze and open field tests revealed that gelsevirine significantly alleviated cognitive dysfunction and increased exploratory behaviour in mice with SAE. Gelsevirine inhibited the activation of microglia and decreased inflammatory factor levels in the hippocampus of mice with SAE. In mice with SAE and in vitro BV2 microglia, gelsevirine reduced levels of inflammatory factors and inhibited STING protein phosphorylation and microglial pyroptosis. However, after STING knockout, the inhibitory effect of gelsevirine on microglial pyroptosis was significantly weakened, and gelsevirine-mediated protective effects were abolished.</div></div><div><h3>Conclusions</h3><div>Gelsevirine increased the survival rate, ameliorated cognitive impairment, inhibited glial cell activation and reduced inflammation in the hippocampi of mice with SAE; the mechanism may be related to the inhibition of STING signalling pathway-mediated pyroptosis in microglia.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142319841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sishen pills inhibit inflammatory dendritic cell differentiation via miR-505–3p mediated E-cadherin downregulation in ulcerative colitis","authors":"","doi":"10.1016/j.phymed.2024.156035","DOIUrl":"10.1016/j.phymed.2024.156035","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Ulcerative colitis (UC) is an autoimmune disease that is highly susceptible to recurrence, which is still a lack of effective drugs with minor side effects in clinic. Intervention of inflammatory differentiation of dendritic cells (DCs) might be an effective strategy to treat UC. Sishen Pills (SSP) is a classic Chinese herbal formula which has been demonstrated the protective effect of UC, but the mechanism remains unclear.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Purpose&lt;/h3&gt;&lt;div&gt;To elucidate the protective effects of SSP against UC in mice and reveal its regulatory mechanism of DCs and the key active ingredients for the UC treatment based on transcriptomics, network pharmacology and experiments validation in &lt;em&gt;vivo&lt;/em&gt; and &lt;em&gt;vitro&lt;/em&gt;.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Method&lt;/h3&gt;&lt;div&gt;The key active ingredients of SSP were detected and screened integrating LC-MS/MS and network pharmacology. A mouse UC model was induced with 3% sodium dextran sulfate and treated with SSP for 14 days to evaluate the efficacy. ELISA was used to detect the levels of IL-6, IL-1β and TNF-α in the colon; flow cytometry was used to detect the expression levels of DCs and their subpopulations; whole transcriptomic sequencing of differential RNAs in the colon and RT-PCR to detect key miRNAs to verify the sequencing results. Mouse bone marrow-derived dendritic cells (BMDCs) were isolated, an inflammatory model was constructed using 100 ng/ml LPS, and the effects of SSP on DC proliferation and apoptosis and their surface co-stimulatory molecule expression were examined; IL-6, IL-1β, TNF-α levels were measured by ELISA; RT-PCR and WB were performed to detect &lt;em&gt;miR-505–3p, CDH1&lt;/em&gt;, E-cadherin expression. BMDCs with low expression of miR-505–3p were constructed by lentiviral transfection for further validation. The potential key ingredient was re-validated in &lt;em&gt;vivo&lt;/em&gt; and &lt;em&gt;vitro&lt;/em&gt; experiment.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Animal experiments showed that SSP alleviated DSS-induced UC symptoms and colonic pathological injury in mice, and inhibited IL-6, IL-1β, TNF-α secretion and inflammatory DC proliferation and activation maturation. Network pharmacology predicted that evodiamine, isobavachalcone, curcumin, and engenol may play a key role in SSP. RNA sequencing revealed that &lt;em&gt;miR-505–3p&lt;/em&gt;, as the differential miRNA, shared a large number of transcription factors with E-cadherin, and was involved in inflammatory differentiation regulation. In &lt;em&gt;vivo&lt;/em&gt; experiments confirmed that SSP accelerated apoptosis, slowed down proliferation, inhibited inflammatory differentiation and IL-6, IL-1β, and TNF-α secretion in BMDCs, and decreased &lt;em&gt;miR-505–3p, CDH1&lt;/em&gt;, and E-cadherin levels. After knocking down &lt;em&gt;miR-505–3p&lt;/em&gt;, SSP could not regulate the inflammatory differentiation and IL-6, IL-1β, TNF-α level in BMDCs. Additionally, evodiamine was found and verified to be the key active ingredient of SSP in preventing the inflammatory differatiation of ","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142352545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Huang-Jin-Shuang-Shen Decoction promotes CD8+ T-cell-mediated anti-tumor immunity by regulating chemokine CXCL10 in gastric cancer","authors":"","doi":"10.1016/j.phymed.2024.156065","DOIUrl":"10.1016/j.phymed.2024.156065","url":null,"abstract":"<div><h3>Background</h3><div>Research on immunotherapy for gastric cancer is currently receiving significant attention, with particular emphasis on the role of CD8+ <em>T</em> cells in anti-tumor immune responses. In recent years, the importance of the chemokine CXCL10 in promoting anti-tumor immunity has been increasingly recognized because it plays a crucial role in recruiting CD8+ <em>T</em> cells to the tumor microenvironment. The Huang-Jin-Shuang-Shen (HJSS) Decoction, a Chinese medicine, has been used as an adjuvant drug for gastric cancer chemotherapy. Its mechanism of action may be related to the activation of anti-tumor immunity.</div></div><div><h3>Purpose</h3><div>To assess the role of the HJSS Decoction in regulating the immune microenvironment of gastric cancer and elucidate its mechanism.</div></div><div><h3>Study design/methods</h3><div>Ultra-high performance liquid chromatography Q Exactive-mass spectrometry was used to analyze the main components of the HJSS Decoction and evaluate the therapeutic effect of the HJSS Decoction synergized with 5-fluorouracil (5-FU) on gastric cancer. The proportions of CD8+ <em>T</em> cells and killing markers were determined using flow cytometry. Mechanisms of action and targets were screened using network pharmacology. The level of CXCL10 was detected using enzyme-linked immunosorbent assay and western blot, and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) related signaling pathway was detected <em>in vitro</em>. The target function was validated by siRNA transfection.</div></div><div><h3>Results</h3><div>The combination of HJSS Decoction and 5-FU demonstrated a synergistic effect in impeding the progression of subcutaneous gastric cancer. This was achieved through the facilitation of apoptosis and suppression of proliferation. Furthermore, HJSS Decoction exhibited the ability to enhance the population of CD8+ <em>T</em> cells and augment their cytotoxic capabilities, both in laboratory settings and in living organisms. Notably, HJSS Decoction upregulated the expression of CXCL10, and mechanistically, it activated the NFκB-related signaling pathway to initiate subsequent transcription of chemokines.</div></div><div><h3>Conclusion</h3><div>The present study aimed to investigate the pharmacological mechanism of the HJSS Decoction and its potential clinical application in inhibiting gastric cancer in mice. HJSS Decoction can cooperate with 5-FU to inhibit gastric cancer, and the optimal dose is medium. HJSS Decoction exerts anti-tumor immunity by activating the NFκB-related signaling pathway and promoting the expression of CXCL10, which in turn recruits CD8+ <em>T</em> cells into the tumor immune microenvironment. Overall, these findings provide valuable evidence for the potential clinical application of HJSS Decoction.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142352540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Hesperetin promotes DOT1L degradation and reduces histone H3K79 methylation to inhibit gastric cancer metastasis\" [Phytomedicine 84 (2021) 153499/PMID: 33667841].","authors":"Si-Wei Wang, Hao Sheng, Fang Zheng, Feng Zhang","doi":"10.1016/j.phymed.2024.155998","DOIUrl":"https://doi.org/10.1016/j.phymed.2024.155998","url":null,"abstract":"","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142293607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into the anticancer effects of galangal and galangin: A comprehensive review","authors":"","doi":"10.1016/j.phymed.2024.156085","DOIUrl":"10.1016/j.phymed.2024.156085","url":null,"abstract":"<div><h3>Backgrounds</h3><div>Cancer continues to be the leading cause of death worldwide, significantly impacting both health and the economy. Natural products have emerged as promising sources for the development of new anticancer drugs, with galangal and their active ingredient, galangin, garnering substantial interest.</div></div><div><h3>Purpose</h3><div>This study summarizes recent findings on the anticancer properties of galangal and galangin, highlighting their potential to target various cancer types.</div></div><div><h3>Methods</h3><div>We systematically searched the literature across PubMed, Web of Science, and Google Scholar, using keywords such as “<em>Alpinia officinarum</em>,” “<em>Alpinia galanga</em>”, “galangal,” and “galangin.” This thorough approach allowed us to gather and compile a comprehensive collection of existing research on the topic.</div></div><div><h3>Results</h3><div>This article provided a thorough analysis of the distribution of galangal, the methods used to extract the active compounds of galangal, and the anticancer properties of both galangin and galangal. It is important to note that galangal and galangin primarily function by regulating the signaling pathways of PI3K/Akt, MAPK, AMPK, p53, NF-κB, and Ras/RAF/MEK/ERK, which in turn triggers apoptosis, autophagy, and ROS while preventing the migration and invasion of cancer cells. We also discussed their toxicity, bioavailability, and clinical uses.</div></div><div><h3>Conclusion</h3><div>In conclusion, galangal extract and galangin have a lot of promise for treating cancer. It is anticipated that this review will further advance the use of galangal extract and galangin as potential cancer treatment medications. Moreover, the discovery and development of drugs based on galangal has enormous potential for the therapy of cancer.</div></div>","PeriodicalId":20212,"journal":{"name":"Phytomedicine","volume":null,"pages":null},"PeriodicalIF":6.7,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142358166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}