Objective Osteogenesis is vitally important for bone defect repair,and Zuo Gui Wan(ZGW)is a classic prescription in traditional Chinese medicine(TCM)for strengthening bones.However,the specific mechanism by which ZGW ...Objective Osteogenesis is vitally important for bone defect repair,and Zuo Gui Wan(ZGW)is a classic prescription in traditional Chinese medicine(TCM)for strengthening bones.However,the specific mechanism by which ZGW regulates osteogenesis is still unclear.The current study is based on a network pharmacology analysis to explore the potential mechanism of ZGW in promoting osteogenesis.Methods A network pharmacology analysis followed by experimental validation was applied to explore the potential mechanisms of ZGW in promoting the osteogenesis of bone marrow mesenchymal stem cells(BMSCs).Results In total,487 no-repeat targets corresponding to the bioactive components of ZGW were screened,and 175 target genes in the intersection of ZGW and osteogenesis were obtained.And 28 core target genes were then obtained from a PPI network analysis.A GO functional enrichment analysis showed that the relevant biological processes mainly involve the cellular response to chemical stress,metal ions,and lipopolysaccharide.Additionally,KEGG pathway enrichment analysis revealed that multiple signaling pathways,including the phosphatidylinositol-3-kinase/protein kinase B(PI3K/AKT)signaling pathway,were associated with ZGW-promoted osteogensis.Further experimental validation showed that ZGW could increase alkaline phosphatase(ALP)activity as well as the mRNA and protein levels of ALP,osteocalcin(OCN),and runt related transcription factor 2(Runx 2).What’s more,Western blot analysis results showed that ZGW significantly increased the protein levels of p-PI3K and p-AKT,and the increases of these protein levels significantly receded after the addition of the PI3K inhibitor LY294002.Finally,the upregulated osteogenic-related indicators were also suppressed by the addition of LY294002.Conclusion ZGW promotes the osteogenesis of BMSCs via PI3K/AKT signaling pathway.展开更多
This paper tests the hypothesis that the commentary trend of the Shen Nong Ben Cao Jing(Shen Nong’s Classic of the Materia Medica)arises alongside the fashionable philology of the time,or the aversion against the Jin...This paper tests the hypothesis that the commentary trend of the Shen Nong Ben Cao Jing(Shen Nong’s Classic of the Materia Medica)arises alongside the fashionable philology of the time,or the aversion against the Jin-Yuan medical philosophy.After surveying 12 major commentaries,it is concluded that the situation is more complicated than a simple assertion.The seemingly opposite philosophy and philology approaches have been used eclectically to innovate the understanding of ancient traditional Chinese medicine texts.展开更多
Objective:To investigate the therapeutic effect of Bai Hu Ren Shen Soup(BHRSS)on type 2 diabetes mellitus(T2DM)rats and explore whether its therapeutic effect is achieved by promoting autophagy in the pancreas tissue ...Objective:To investigate the therapeutic effect of Bai Hu Ren Shen Soup(BHRSS)on type 2 diabetes mellitus(T2DM)rats and explore whether its therapeutic effect is achieved by promoting autophagy in the pancreas tissue of T2DM rats.Methods:Thirty male standard deviation rats were equally divided into normal control group,T2DM group and BHRSS group.Firstly,the therapeutic effect of BHRSS on T2DM was evaluated by biochemical indices in serum and pathological changes in the pancreas tissue of rats in each group after modeling and medication.Then,the levels of microtubule-associated protein 1 light chain 3(LC3)protein and p62 protein in the pancreas tissue of rats in each group after BHRSS intervention were detected by Western blot.Results:BHRSS intervention significantly reduced the levels of blood sugar,liver and kidney function,and other related biochemical indices in the serum of T2DM rats,and effectively improved the pathological changes in the pancreas tissue of T2DM rats.In addition,Western blot results showed that the expression levels of autophagy-related protein LC3 protein in the pancreas tissue of rats were increased,and the expression level of p62 protein was decreased after BHRSS intervention.Conclusion:BHRSS has a clear therapeutic effect on T2DM model rats,which may be related to that increase of autophagy protein LC3 and the decrease of p62 protein level in the pancreas tissue.展开更多
文摘Objective Osteogenesis is vitally important for bone defect repair,and Zuo Gui Wan(ZGW)is a classic prescription in traditional Chinese medicine(TCM)for strengthening bones.However,the specific mechanism by which ZGW regulates osteogenesis is still unclear.The current study is based on a network pharmacology analysis to explore the potential mechanism of ZGW in promoting osteogenesis.Methods A network pharmacology analysis followed by experimental validation was applied to explore the potential mechanisms of ZGW in promoting the osteogenesis of bone marrow mesenchymal stem cells(BMSCs).Results In total,487 no-repeat targets corresponding to the bioactive components of ZGW were screened,and 175 target genes in the intersection of ZGW and osteogenesis were obtained.And 28 core target genes were then obtained from a PPI network analysis.A GO functional enrichment analysis showed that the relevant biological processes mainly involve the cellular response to chemical stress,metal ions,and lipopolysaccharide.Additionally,KEGG pathway enrichment analysis revealed that multiple signaling pathways,including the phosphatidylinositol-3-kinase/protein kinase B(PI3K/AKT)signaling pathway,were associated with ZGW-promoted osteogensis.Further experimental validation showed that ZGW could increase alkaline phosphatase(ALP)activity as well as the mRNA and protein levels of ALP,osteocalcin(OCN),and runt related transcription factor 2(Runx 2).What’s more,Western blot analysis results showed that ZGW significantly increased the protein levels of p-PI3K and p-AKT,and the increases of these protein levels significantly receded after the addition of the PI3K inhibitor LY294002.Finally,the upregulated osteogenic-related indicators were also suppressed by the addition of LY294002.Conclusion ZGW promotes the osteogenesis of BMSCs via PI3K/AKT signaling pathway.
文摘This paper tests the hypothesis that the commentary trend of the Shen Nong Ben Cao Jing(Shen Nong’s Classic of the Materia Medica)arises alongside the fashionable philology of the time,or the aversion against the Jin-Yuan medical philosophy.After surveying 12 major commentaries,it is concluded that the situation is more complicated than a simple assertion.The seemingly opposite philosophy and philology approaches have been used eclectically to innovate the understanding of ancient traditional Chinese medicine texts.
文摘Objective:To investigate the therapeutic effect of Bai Hu Ren Shen Soup(BHRSS)on type 2 diabetes mellitus(T2DM)rats and explore whether its therapeutic effect is achieved by promoting autophagy in the pancreas tissue of T2DM rats.Methods:Thirty male standard deviation rats were equally divided into normal control group,T2DM group and BHRSS group.Firstly,the therapeutic effect of BHRSS on T2DM was evaluated by biochemical indices in serum and pathological changes in the pancreas tissue of rats in each group after modeling and medication.Then,the levels of microtubule-associated protein 1 light chain 3(LC3)protein and p62 protein in the pancreas tissue of rats in each group after BHRSS intervention were detected by Western blot.Results:BHRSS intervention significantly reduced the levels of blood sugar,liver and kidney function,and other related biochemical indices in the serum of T2DM rats,and effectively improved the pathological changes in the pancreas tissue of T2DM rats.In addition,Western blot results showed that the expression levels of autophagy-related protein LC3 protein in the pancreas tissue of rats were increased,and the expression level of p62 protein was decreased after BHRSS intervention.Conclusion:BHRSS has a clear therapeutic effect on T2DM model rats,which may be related to that increase of autophagy protein LC3 and the decrease of p62 protein level in the pancreas tissue.
