AIM:To exploring the mechanism of Xin Mai Jia(XMJ)in inhibiting hypertensive cardiac hypertrophy through network pharmacology and animal experiments.METHODS:Retrieving the ac-tive ingredients and target points of XMJ by search-ing the TCMSP database and related literature re-ports;using the Gene Cards,OMIM,and Drug Bank databases to screen targets for hypertensive cardi-ac hypertrophy;constructing a network of tradi-tional Chinese medicine-active ingredients-poten-tial targets and a protein-protein interaction(PPI)network;using DAVID software for target gene on-tology(GO)functional enrichment analysis and Kyo-to Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis;using Auto Dock soft-ware for molecular docking.A spontaneously hy-pertensive rat(SHR)model was established,and hematoxylin-eosin(HE)staining was used to detect the morphology of cardiac tissue and cellular hy-pertrophy,Masson staining was used to detect col-lagen deposition in cardiac tissue,and Western blot to detect the expression of heat shock protein(HSP90AA1),mammalian target of rapamycin(mTOR),peroxisome proliferator-activated receptor y(PPARG),and tumor necrosis factor(TNF-α)in car-diac tissue.RESULTS:A total of 56 potential active ingredients were identified in XMJ,and 5,492 tar-gets related to hypertensive cardiac hypertrophy were obtained.The targets in the core network were ranked according to their Degree values,and four main targets were selected:HSP90AA1,mTOR,PPARG,and TNF-α.The results of HE staining showed that compared with the normal group,the average area of cardiomyocytes in the SHR group increased significantly(P＜0.05),while there was no significant change in the XMJ group.The hypertro-phy in the SHR+XMJ group was significantly alleviat-ed(P＜0.05).The results of Masson staining showed that compared with the normal group,the levels of interstitial fibrosis and perivascular fibrosis in the SHR group rats increased significantly(P＜0.01),and XMJ could significantly reduce the fibrosis levels in the SHR group rats(P＜0.01).The results of Western blot showed that compared with the normal group rats,the expression of HSP90AA1 and PPARG in the myocardial tissue of SHR group rats was downregu-lated,mTOR phosphorylation was downregulated,and TNF-α was significantly upregulated(P＜0.01).In the SHR+XMJ group,the expression of HSP90AA1,PPARG,and TNF-α in the myocardial tis-sue of rats returned to normal levels,and mTOR phosphorylation returned to normal levels.In the XMJ group,there were no significant changes in the above indicators compared with the normal group rats.CONCLUSION:The mechanism underly-ing the inhibitory effect of XMJ on myocardial cell hypertrophy in hypertension involves a comprehen-sive action through multiple components,multiple targets,and multiple pathways.

AIM:To exploring the mechanism of Xin Mai Jia(XMJ)in inhibiting hypertensive cardiac hypertrophy through network pharmacology and animal experiments.METHODS:Retrieving the ac-tive ingredients and target points of XMJ by search-ing the TCMSP database and related literature re-ports;using the Gene Cards,OMIM,and Drug Bank databases to screen targets for hypertensive cardi-ac hypertrophy;constructing a network of tradi-tional Chinese medicine-active ingredients-poten-tial targets and a protein-protein interaction(PPI)network;using DAVID software for target gene on-tology(GO)functional enrichment analysis and Kyo-to Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis;using Auto Dock soft-ware for molecular docking.A spontaneously hy-pertensive rat(SHR)model was established,and hematoxylin-eosin(HE)staining was used to detect the morphology of cardiac tissue and cellular hy-pertrophy,Masson staining was used to detect col-lagen deposition in cardiac tissue,and Western blot to detect the expression of heat shock protein(HSP90AA1),mammalian target of rapamycin(mTOR),peroxisome proliferator-activated receptor y(PPARG),and tumor necrosis factor(TNF-α)in car-diac tissue.RESULTS:A total of 56 potential active ingredients were identified in XMJ,and 5,492 tar-gets related to hypertensive cardiac hypertrophy were obtained.The targets in the core network were ranked according to their Degree values,and four main targets were selected:HSP90AA1,mTOR,PPARG,and TNF-α.The results of HE staining showed that compared with the normal group,the average area of cardiomyocytes in the SHR group increased significantly(P＜0.05),while there was no significant change in the XMJ group.The hypertro-phy in the SHR+XMJ group was significantly alleviat-ed(P＜0.05).The results of Masson staining showed that compared with the normal group,the levels of interstitial fibrosis and perivascular fibrosis in the SHR group rats increased significantly(P＜0.01),and XMJ could significantly reduce the fibrosis levels in the SHR group rats(P＜0.01).The results of Western blot showed that compared with the normal group rats,the expression of HSP90AA1 and PPARG in the myocardial tissue of SHR group rats was downregu-lated,mTOR phosphorylation was downregulated,and TNF-α was significantly upregulated(P＜0.01).In the SHR+XMJ group,the expression of HSP90AA1,PPARG,and TNF-α in the myocardial tis-sue of rats returned to normal levels,and mTOR phosphorylation returned to normal levels.In the XMJ group,there were no significant changes in the above indicators compared with the normal group rats.CONCLUSION:The mechanism underly-ing the inhibitory effect of XMJ on myocardial cell hypertrophy in hypertension involves a comprehen-sive action through multiple components,multiple targets,and multiple pathways.

Thyroid carcinoma is closely related to environmental factors. Gene mutations and molecular biological changes of gland tissue caused by environmental changes are important factors inducing thyroid carcinoma. Although the molecular mechanism of thyroid carcinoma has not been fully elucidated,increasingly specific genetic changes and molecular markers for thyroid carcinoma have been discovered with the development of molecular biology techniques. This article reviews the recent progresses on the etiology,specific molecular markers,diagnosis and targeted therapies of thyroid carcinoma,so as to provide theoretical support for the clinical diagnosis and treatment of thyroid carcinoma.