Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-i...Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-induced anorexia was discussed from the aspects of regulating gut microbiota,repairing intestinal barrier injury and inhibiting inflammatory pathways.Methods:A rat model of chemotherapy-induced anorexia was established using cisplatin.The study evaluated the therapeutic effects of LJZD by observing the weight,food intake,and intestinal pathology of rats.The impact of LJZD on gut microbiota and metabolites,specifically short-chain fatty acids,was investigated through gut microbiota analysis and targeted metabolomics.The anti-inflammatory and intestinal protective effects of LJZD were assessed by examining the expression of intestinal tight junction proteins associated with the inflammatory pathway.Results:LJZD alleviated cisplatin-induced inflammation and intestinal barrier disruption,as evidenced by upregulated expression of tight junction protein 1(TJ-1)and occludin,along with reduced serum levels of interleukin 6(IL-6),interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and lipopolysaccharide.Additionally,LJZD alleviated microbiota imbalance and regulated the levels of short-chain fatty acids,especially increased the relative abundance of Coriobacteriales Incertae Sedis,Lactabacillus johnsonii F19785,Parasutterella,and reduced the Tyzzerella.In the hypothalamus,LJZD exerts suppressive effects on the toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)p65 signaling pathway,leading to a downregulation in the transcriptional activity of IL-6 and IL-1β,as well as Interleukin 6 receptors(IL-6R)and Interleukin-1βreceptors(IL-1R1)mRNA expression levels.Conclusion:In summary,LJZD alleviate chemotherapy-induced anorexia by modulating the gut microbiota,repairing the intestinal mechanical barriers,and suppressing the TLR4/MyD88/NF-κB p65 signaling pathway.展开更多
Objective:To investigate the relationship among Pokemon,NF-κB p65 and Bcl-2 in hepatoma cells.Methods:HCC cell HepG2,SMMC7721 and human fetal liver cell line L02 cells were used,and expression of Pokemon,NF-κB p65 a...Objective:To investigate the relationship among Pokemon,NF-κB p65 and Bcl-2 in hepatoma cells.Methods:HCC cell HepG2,SMMC7721 and human fetal liver cell line L02 cells were used,and expression of Pokemon,NF-κB p65 and Bcl-2 in three cells were detected by realtime PCR and western blot.Then siRNA of Pokemon was applied to inhibit the expression of Pokemon and NF-κB p65 and apoptotic rate was determined by flow cytometric analysis. Results:Expressions of Pokemon,NF-κB p65 and Bcl-2 in human hepatoma cell HepG2, SMMC7721 expression were significantly higher than those in human embryonic stem cells L02. siRNA of Pokemon inhibited the expression of Pokemon,NF-κB p65 and Bcl-2 in liver cancer cells,and significantly increased apoptosis of liver cells.While siRNA of NF-κB n65 inhibited the expression of NF-κB p65 and Bcl-2,but Pokemon expression in hepatoma cells had no significant change.Conclusions:The proto-oncogene Pokemon can inhibit PI4ARF by specific transcription regulation of cell cycle and can induce tumors.In addition,Pokemon can regulate NF-κB p65 through the expression of apoptosis repressor,and promote the development of liver cancer.It suggests signal network in the liver include the regulation of new non-classical NF-κB regulatory pathway.展开更多
基金National Natural Science Foundation of China(grant numbers 82174143)the Innovative Team Project of Ordinary Universities in Guangdong Province(grant numbers 2022KCXTD016).
文摘Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-induced anorexia was discussed from the aspects of regulating gut microbiota,repairing intestinal barrier injury and inhibiting inflammatory pathways.Methods:A rat model of chemotherapy-induced anorexia was established using cisplatin.The study evaluated the therapeutic effects of LJZD by observing the weight,food intake,and intestinal pathology of rats.The impact of LJZD on gut microbiota and metabolites,specifically short-chain fatty acids,was investigated through gut microbiota analysis and targeted metabolomics.The anti-inflammatory and intestinal protective effects of LJZD were assessed by examining the expression of intestinal tight junction proteins associated with the inflammatory pathway.Results:LJZD alleviated cisplatin-induced inflammation and intestinal barrier disruption,as evidenced by upregulated expression of tight junction protein 1(TJ-1)and occludin,along with reduced serum levels of interleukin 6(IL-6),interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and lipopolysaccharide.Additionally,LJZD alleviated microbiota imbalance and regulated the levels of short-chain fatty acids,especially increased the relative abundance of Coriobacteriales Incertae Sedis,Lactabacillus johnsonii F19785,Parasutterella,and reduced the Tyzzerella.In the hypothalamus,LJZD exerts suppressive effects on the toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)p65 signaling pathway,leading to a downregulation in the transcriptional activity of IL-6 and IL-1β,as well as Interleukin 6 receptors(IL-6R)and Interleukin-1βreceptors(IL-1R1)mRNA expression levels.Conclusion:In summary,LJZD alleviate chemotherapy-induced anorexia by modulating the gut microbiota,repairing the intestinal mechanical barriers,and suppressing the TLR4/MyD88/NF-κB p65 signaling pathway.
文摘Objective:To investigate the relationship among Pokemon,NF-κB p65 and Bcl-2 in hepatoma cells.Methods:HCC cell HepG2,SMMC7721 and human fetal liver cell line L02 cells were used,and expression of Pokemon,NF-κB p65 and Bcl-2 in three cells were detected by realtime PCR and western blot.Then siRNA of Pokemon was applied to inhibit the expression of Pokemon and NF-κB p65 and apoptotic rate was determined by flow cytometric analysis. Results:Expressions of Pokemon,NF-κB p65 and Bcl-2 in human hepatoma cell HepG2, SMMC7721 expression were significantly higher than those in human embryonic stem cells L02. siRNA of Pokemon inhibited the expression of Pokemon,NF-κB p65 and Bcl-2 in liver cancer cells,and significantly increased apoptosis of liver cells.While siRNA of NF-κB n65 inhibited the expression of NF-κB p65 and Bcl-2,but Pokemon expression in hepatoma cells had no significant change.Conclusions:The proto-oncogene Pokemon can inhibit PI4ARF by specific transcription regulation of cell cycle and can induce tumors.In addition,Pokemon can regulate NF-κB p65 through the expression of apoptosis repressor,and promote the development of liver cancer.It suggests signal network in the liver include the regulation of new non-classical NF-κB regulatory pathway.
