详细信息
Intervention effect of Cigu Xiaozhi prescription on ceramide lipoapoptosis in non-alcoholic fatty liver disease ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Intervention effect of Cigu Xiaozhi prescription on ceramide lipoapoptosis in non-alcoholic fatty liver disease
作者:Yang, Shaojun[1];Ma, Yanhua[2];Bai, Zhouxia[3];Yu, Ye[1];Fang, Buwu[4];Zhang, Li[4];Wang, Li[2]
第一作者:Yang, Shaojun
通信作者:Yang, SJ[1];Ma, YH[2]
机构:[1]Beihai Tradit Chinese Med Hosp, Dept Spleen & Stomach Dis, Beihai 536000, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Clin Med Coll 1, Lanzhou 730000, Peoples R China;[3]Gansu Univ Tradit Chinese Med, Affiliated Hosp, Dept Clin Lab, Lanzhou 730000, Peoples R China;[4]Tianjin Med Univ, Sch Basic Med, Dept Pharmacol, Tianjin 300070, Peoples R China
第一机构:Beihai Tradit Chinese Med Hosp, Dept Spleen & Stomach Dis, Beihai 536000, Peoples R China
通信机构:[1]corresponding author), Beihai Tradit Chinese Med Hosp, Dept Spleen & Stomach Dis, Beihai 536000, Peoples R China;[2]corresponding author), Gansu Univ Tradit Chinese Med, Clin Med Coll 1, Lanzhou 730000, Peoples R China.|[10735]甘肃中医药大学;
年份:2024
卷号:44
期号:1
起止页码:63
外文期刊名:JOURNAL OF TRADITIONAL CHINESE MEDICINE
收录:;WOS:【SCI-EXPANDED(收录号:WOS:001179683200001)】;
语种:英文
外文关键词:non-alcoholic fatty liver disease; ceramides; Cigu Xiaozhi prescription; detoxification and phlegm removal
摘要:OBJECTIVE: To explore the mechanism of the Chinese medicine Cigu Xiaozhi prescription ((sic)(sic)(sic), CGXZ) in the treatment of the non-alcoholic fatty liver disease (NAFLD) by detoxification and phlegm-reducing, the effect of CGXZ prescription on ceramide-mediated lipid apoptosis in Hep G2 cells with NAFLD. METHODS: The experiment was randomly divided into 6 groups: normal control group, model group, CGXZ prescription medicated serum high, medium, and low dose groups, and pioglitazone positive control group. Using 500 mu mol/L free fatty acid (FFA) mixture to induce Hep G2 cells to establish NAFLD cell model, respectively, with 2%, 4%, and 6% concentration of CGXZ prescription medicated serum intervention for 24 h. The changes in organelles and lipid droplet accumulation were observed under the electron microscope. Furthermore, TdT-mediated dUTP Nick-End Labeling method was used to assay hepatocyte apoptosis; Biochemical determination of glutamic-pyruvic transaminase, glutamic oxalacetic transaminase, triglycerides, and FFA levels in Hep G2 cells; the content of ceramide was determined by high- performance thin-layer chromatography. Finally, Western Blot and quantitative real-time polymerase chain reaction (qRT-PCR) were used to determine the protein and gene expression levels, such as inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-kappa B), B cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (Bax). RESULTS: Under the electron microscope, the cells in the model group showed moderate-to-severe steatosis, and apoptotic bodies could be seen. The model group had greater improvements in the apoptosis rate (P < 0.01), and the levels of ceramide C2 and FFA in the cytoplasm (P < 0.01) than the normal control group. The protein expressions of NF-kappa B, iNOS, and Bax were significantly up-regulated (P < 0.05), while the Bcl-2 had no significant change (P > 0.05). Compared with the model group, the levels of ceramide C2 and FFA (P < 0.01), the protein expressions of NF-kappa B, iNOS, and Bax (P < 0.05) in the CGXZ prescription treatment group and pioglitazone positive control group were significantly decreased; Only the Bcl-2 protein was significantly up-regulated in the high-dose Chinese medicine group (P < 0.05). The down -regulation of Bax mRNA expression in each Chinese medicine treatment group was significantly better than in the pioglitazone positive control group (P < 0.01). CONCLUSIONS: The CGXZ prescription, formulated with the method of detoxification and phlegm, can inhibit lipoapoptosis in the NAFLD cell model by down -regulating the levels of ceramide C2 and FFA, which may be achieved by regulating ceramide/iNOS/NF-kappa B signaling pathway. (c) 2024 JTCM. All rights reserved.
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