BACKGROUND:Chaihu-Shugan-San (CSS), a classic traditional Chinese medicine formula, has demonstrated significant efficacy in treating various gastrointestinal disorders. AIM:To explore the therapeutic efficacy of CSS in alleviating chronic atrophic gastritis (CAG), and elucidate the underlying mechanisms of action. METHODS:High performance liquid chromatography-mass spectrometry was used to identify the main active components of CSS. The therapeutic effects of CSS at doses of 925 mg/kg/day and 1850 mg/kg/day on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced CAG were evaluated. Network pharmacology and molecular docking were used to predict the potential targets of CSS in CAG. The impact of CSS on the gut microbiota of rats was investigated by 16S rRNA sequencing. RESULTS:The main active components of CSS were lipids and lipid-like molecules, phenylpropanoids and polyketides. In vivo experiments showed that CSS significantly ameliorated MNNG-induced CAG by inhibiting inflammation and apoptosis. The core target of CSS to alleviate CAG were tumor necrosis factor, interleukin (IL)-1β, IL-6, BAX, BCL2, caspase-3/caspase-9, and NFKBIA. Gene Ontology analysis of these core targets revealed their predominant association with the nuclear factor-kappa B (NF-κB) signaling complex and BAX apoptotic complex. Molecular docking demonstrated that six compounds in CSS, including baicalin, licoisoflavone B, licochalcone B, glabrone, glycyrrhiza flavonol A, and marmin exhibited strong binding affinities with NFKBIA. 16S rRNA sequencing indicated that CSS promoted beneficial changes in the colonic microbial community. CONCLUSION:CSS alleviated CAG by inhibiting NF-κB-mediated inflammation and apoptosis, providing insights into its mechanism of action in protection against CAG.

Nobiletin is one of the citrus polymethoxyflavones and exhibits antioxidant and anti-inflammatory properties. Nobiletin is reportedly used to mitigate ethanol-induced gastric injury and to inhibit Helicobacter pylori infection-related gastric tumorigenesis. The present study aims to elucidate whether and how nobiletin exerts gastroprotective effects in N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced chronic atrophic gastritis (CAG). In MNNG-induced Sprague-Dawley (SD) rats with CAG, we found that nobiletin dose-dependently alleviated MNNG-induced gastric histological lesions, overgeneration of inflammatory cytokines, and intestinal metaplasia. The potential targets of nobiletin in the treatment of CAG were predicted through metabolomic analysis and network pharmacology and subsequently verified by molecular docking and cell experiments. The results demonstrated that nobiletin alleviates MNNG-induced gastric epithelial cell injury and mitochondrial dysfunction by targeting arachidonate 5-lipoxygenase (ALOX5) and prostaglandin-endoperoxide synthase 2 (PTGS2). In conclusion, nobiletin alleviates MNNG-induced gastric injury in vivo and the damage of GES-1 cells in vitro via ALOX5 and PTGS2.

Ethnopharmacological relevance: Traditional Chinese medicine (TCM) theory believes that clearing heat and promoting dampness is the main treatment method for chronic gastritis. Coptis chinensis Franch. has the effects of clearing heat, detoxifying, and anti-inflammatory; Magnolia officinalis var. biloba can be used to treat abdominal pain, cough, and asthma. Coptis chinensis Franch. and Magnolia officinalis var. biloba can regulate the balance of intestinal microbiota and inhibit inflammatory reactions. Aim: This study will verify the therapeutic effect of Coptis chinensis Franch. and Magnolia officinalis var. biloba on chronic gastritis, and explore its mechanism through transcriptome sequencing. Methods: Firstly, a rat chronic gastritis model was established, and the anal temperature and body weight changes of the rats before and after modeling were observed. Next, H & E staining, TUNEL assay and ELISA assay were performed on rat gastric mucosal tissues. Subsequently, the key fractions of Coptis chinensis Franch. and Magnolia officinalis var. biloba were obtained by high performance liquid chromatography (HPLC), and a GES-1 cell inflammation model was constructed to select the optimal monomer. Finally, the mechanism of action of Coptis chinensis Franch. and Magnolia officinalis var. biloba was explored through RNA seq. Results: Compared with the control group, the rats in the administered group were in better condition, with higher anal temperature, reduced inflammatory response in gastric mucosal tissue and reduced apoptosis. The optimal fraction Coptisine was subsequently determined by HPLC and GES-1 cell model. RNA-seq analysis revealed that DEG was significantly enriched in ribosomes, NF-& kappa;B signaling pathway, etc. The key genes TPT1 and RPL37 were subsequently obtained. Conclusions: This study verified the therapeutic effects of Coptis chinensis Franch. and Magnolia officinalis var. biloba on chronic gastritis by in vivo and in vitro experiments in rats, identified Coptisine as the optimal component, and obtained two potential target genes.

目的 文章基于网络药理学和分子对接的方法,探究藏药"甘松-余甘子"治疗幽门螺杆菌相关胃炎的相关作用机制.方法 运用TCMSP,获得藏药"甘松-余甘子"活性成分及相关的作用靶点,应用GeneCards、OMIM、DisGeNET数据库获得幽门螺杆菌相关胃炎相关靶点,绘制韦恩图获取药物疾病共同靶点,将其输入Cytoscape 3.7.2软件绘制"药物-成分-疾病-靶点"网络.运用R语言及Cytoscape 3.7.2软件构建蛋白相互作用PPI网络.通过R语言对靶点基因进行GO、KEGG集分析.分别采用AutoDock软件、Pymol软件进行分子对接、可视化验证.结果 藏药"甘松-余甘子"通过15个有效成分作用于16个幽门螺杆菌相关胃炎治疗靶点.筛选出4种核心有效成分,4个核心靶点包括PTGS2、TNF、CASP3、TP53.GO富集分析主要涉及神经元死亡调节、神经元死亡、电离辐射响应、糖皮质激素反应、对紫外线的反应、内在的凋亡信号通路、皮质类固醇反应等生物过程进行调节,KEGG富集分析主要涉及P53信号通路、HIF-1信号通路、TNF信号通路.4种核心有效成分与主要核心靶点PTGS2、TNF、CASP3、TP53均具有一定的结合活性.结论 藏药"甘松-余甘子"治疗幽门螺杆菌相关胃炎的机制,可能是通过"多成分-多靶点-多通路",发挥抗炎、抗癌、抗氧化、抗凋亡、促进血管生成的作用.

Tiaoganquzhi Decoction (TGQZD) is a traditional Chinese herbal formulation demonstrated to be a clinically effective treatment for nonalcoholic fatty liver disease (NAFLD), although details concerning its clinical mechanism are poor. This study aimed to explore the mechanism of TGQZD on improvement of inflammatory damage and dyslipidemia caused by NAFLD through the CGI-58/ROS/NLRP3 inflammasome pathway. In our research, the in vivo protective effects of TGQZD on HFD-induced liver injury in rats and in vitro using lipopolysaccharide (LPS)+palmitate (PA)-stimulated HepG-2 cells model. Histological changes were evaluated by hematoxylin-eosin and Oil Red O staining. Inflammatory cytokines and protein expression were analyzed by ELISA, Real time PCR and western blotting. Liver function, blood lipids, free fatty acids (FFA), and reactive oxygen species (ROS) were determined by biochemical detection. Our results indicated that TGQZD exhibited anti-inflammatory activity, reduced the severity of NAFLD and ameliorated the pathological changes. Further, TGQZD improved liver function and lipid metabolism in NAFLD rats. TGQZD lowered serum aspartate aminotransferase, alanine aminotransferase, triglyceride, and total cholesterol levels. TGQZD suppressed the formulation of FFA and ROS. It also reduced the expression and release of the inflammatory cytokine interleukin-1β by promoting CGI-58 expression and inhibiting the expression of FFA, TNF-α, and the NLRP3 inflammasome induced by ROS. TGQZD exhibited anti-inflammatory effects via the CGI-58, ROS and NLRP3 inflammasome pathway in vivo and in vitro, respectively. Our findings demonstrated that TGQZD is a useful and effective therapeutic agent for treating NAFLD via promotion of CGI-58 to inhibit the expression of ROS-induced NLRP3 inflammasome.

目的 观察健脾清化汤对甲硝唑耐药幽门螺杆菌(Hp)体外生长的影响及菌体内甲硝唑含量的变化,探讨健脾清化汤发挥作用的可能机制.方法 选取甲硝唑耐药Hp临床菌株.实验组利用1、1/2、1/4、1/8、1/16、1/32倍健脾清化汤对Hp的生长及活动进行干预,对照组利用生理盐水进行对比,通过琼脂稀释法及Elisa法观察经2组药物作用后甲硝唑耐药Hp体外的生长情况及菌体内甲硝唑含量的变化.结果 体外抑菌试验显示,1、1/2、1/4倍健脾清化汤对甲硝唑耐药Hp的生长具有抑制作用,其最低抑菌浓度为1/4倍浓度;Elisa法结果显示,较对照组,经健脾清化汤作用后的各组耐药Hp内甲硝唑含量均显著上升,呈梯度变化,各组之间差异有统计学意义(P＜0.05).结论 1、1/2、1/4倍健脾清化汤的能够抑制甲硝唑耐药Hp的生长,同时不同浓度健脾清化汤均能改变菌体内甲硝唑含量,其机制可能与影响Hp外排泵有关.

Context: Jian Pi Qing Chang Hua Shi decoction (JPQCHSD) has been considered as an effective remedy for the treatment of inflammatory bowel disease (IBD) in Chinese traditional medicine. Objective: We evaluated the efficacy of JPQCHSD on 2-4-6-trinitrobenzene sulphonic acid (TNBS)-induced IBD rats and the responsible mechanisms. Materials and methods: Except the rats of the control group (50% ethanol), Sprague-Dawley rats (180 +/- 20 g) induced by TNBS (150 mg/kg in 50% ethanol), received water extract of JPQCHSD daily at 0, 9.5, 19, or 38 g/kg for 12 days. The rats were sacrificed, and their colons were removed to evaluate the disease activity index. Malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO), immunoglobulin A (IgA), tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6, and nuclear factor-kappa B were evaluated. Results: JPQCHSD extract significantly reduced the disease activity index of TNBS-induced colitis with a median effective dose (ED50) of 26.93 g/kg. MPO and MDA were significantly reduced in the 19 and 38 g/kg groups (ED50 values 37.38 and 53.2 g/kg, respectively). The ED50 values for the increased SOD and IgA were 48.98 and 56.3 g/kg. ED50 values for inhibition of TNF-alpha, IL-1 beta, and IL-6 were 32.66, 75.72, and 162.06 g/kg, respectively. Discussion: JPQCHSD promoted mucosal healing in IBD rats via its anti-inflammation, immune regulation, and antioxidation properties. Conclusions: JPQCHSD has healing function on IBD. Further clinical trials are needed to demonstrate its efficacy and tolerance to IBD.

Objective: to analyze the distribution characteristics of major enteropathogens in infectious diarrhea cases attending the intestinal outpatient clinic of Beijing Traditional Chinese medicine hospital, Capital Medical University. Methods: From 2016 to 2019, 588 fecal samples of patients with infectious diarrhea in Beijing Hospital of traditional Chinese Medicine Affiliated to Capital Medical University were collected for microbial isolation, culture, identification and pathogen gene detection. Using VITEK 2 compact full-automatic microbial identification/drug sensitivity analysis system to identify the bacteria isolated from the culture; using serum agglutination test to classify the pure colonies; using multiple fluorescence quantitative PCR amplification technology to detect the gene amplification of the samples. Results: In 2016-2019, the total physical examination rate of pathogen was 39.796%. The top three pathogen were diarrhea Escherichia coli (21.769%, n=128), Salmonella (5.782%, n=34), Vibrio (4.762%, n=28). The difference of positive rates of different pathogens in four years was statistically significant (P=0.021), and the peak of incidence was from July to September. The positive rate of norovirus was 5.612% (n=33), and the highest incidence occurred in May. Conclusion: The pathogen of infectious diarrhea patients in Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University from April to October 2016-2019 is mainly diarrhea Escherichia coli, and the pathogen type of norovirus is GⅡ genome.

Transplantation of bone marrow mesenchymal stem cells has attracted more and more attention as a regenerative therapy for the treatment of liver diseases. A large number of studies have shown that this kind of cells can inhibit the activation of hepatic stellate cells and regulate tissue homeostasis and immune system via a variety of ways. Meanwhile, bone marrow mesenchymal stem cells can inhibit apoptosis of hepatocyte, improve liver function, and reduce inflammation through multiple pathways. These cells have a broad prospect in the treatment of liver cirrhosis. At present, there are many studies on the specific mechanism of bone marrow mesenchymal stem cells transplantation in the treatment of liver cirrhosis. This paper reviews the pathogenesis of liver cirrhosis and the mechanism of bone marrow mesenchymal stem cells transplantation in the treatment of liver cirrhosis, discusses the effectiveness of traditional Chinese medicine method in enhancing the efficacy of bone marrow mesenchymal stem cells transplantation, and looks forward to its application prospect in the future.

Objective To explore the effect of Tangshen Formula ((sic), TSF), a Chinese herbal medicine, on interstitial cells of Cajal (ICC) in the colon of diabetic rats. Methods Fifty-four male Wistar rats were randomly divided into normal control (NC, n=14) and high-fat diet (HFD) groups (n=40). After 6 weeks, the rats in the HFD group were injected intraperitoneally streptozotocin once (30 mg/kg). Thirty rats with fasting blood glucose higher than 11.7 mmol/L were randomly divided into diabetes (DM) and TSF groups, 15 rats in each group. Rats in the NC and DM groups were intragastrically administered with saline, and those in the TSF group were given with TSF (2.4 g/kg) once daily for 20 weeks. Expression levels of Bax, Bcl-2, and caspase-3 in colonic smooth muscle layer were measured by Western blotting and immunohistochemical staining. The number of ICC was determined by immunohistochemical staining. Immunofluorescence was used for analyzing the ratio of classically activated macrophages (M1) and alternatively activated macrophages (M2) to total macrophages. Electron microscopy was used to observe the epithelial ultrastructure and junctions. Results TSF appeared to partially prevented loss of ICC in DM rats (P<0.05). Compared with the NC group, expression levels of Bcl-2, Bax, caspase-3, and TNF-alpha as well as the ratio of M1 to total macrophages increased in DM rats (all P<0.05), and the ratio of M2 to total macrophages decreased (PP<0.01). Compared with the DM group, TSF decreased the expression levels of abovementioned proteins and restore M2 to total macrophages ratio (PP<0.01). TSF appeared to attenuate the ultrastructural changes of epithelia and improve the tight and desmosome junctions between epithelia reduced in the DM rats. Conclusion Reduced number of ICC in DM rats may be associated with damage of the intestinal barrier. The protective effects of TSF on ICC may be through repair of the epithelial junctions, which attenuates inflammation and inflammation-initiated apoptosis in colon of DM rats.

目的:探索清肠化湿汤对5种肠道细菌(双歧杆菌、鼠李唐乳杆菌、大肠杆菌、金黄色葡萄球菌、沙门氏菌)体外增殖与抑制效果,为清肠化湿汤治疗溃疡性结肠炎提供实验依据.方法:针对溃疡性结肠炎活动期紊乱的肠道菌群,采用光电比色法测定清肠化湿汤对双歧杆菌、鼠李唐乳杆菌益生菌的增殖的影响;同时通过试管二倍稀释法测定清肠化湿汤对大肠杆菌、金黄色葡萄球菌、沙门氏菌致病菌最低抑菌浓度(MIC)与最低杀菌浓度(MBC).结果:清肠化湿汤可明显促进双歧杆菌、鼠李唐乳杆菌增殖,抑制大肠杆菌、金黄色葡萄球菌及沙门氏菌,并有效杀灭大肠杆菌、金黄色葡萄球菌.结论:清肠化湿汤可通过促进益生菌生,抑制并杀灭致病菌,恢复肠道菌群平衡,治疗溃疡性结肠炎.

目的 观察参苓白术散对非酒精性脂肪性肝病(NAFLD)模型大鼠血脂、瘦素和胰岛素抵抗的影响,探讨其相关作用机制.方法 20只实验大鼠随机分为正常组5只(正常饲料喂养)和高脂饮食组15只,高脂饮食组大鼠给予高脂饲料喂养制作NAFLD模型,将成模大鼠随机分为模型组、参苓白术散组和吡格列酮组,每组5只,正常组和模型组给予生理盐水灌胃,参苓白术散组给予参苓白术散水煎液灌胃,吡格列酮组给予吡格列酮混悬液灌胃.药物干预8周后进行口服葡萄糖耐量实验,检测大鼠糖耐量变化及血清转氨酶、血脂、瘦素与胰岛素水平,并计算胰岛素抵抗指数.结果 与正常组比较,模型组大鼠血清转氨酶、血脂、瘦素、胰岛素、血糖和胰岛素抵抗指数均显著升高(P＜0.05);与模型组比较,参苓白术散组和吡格列酮组大鼠血清转氨酶、血脂、瘦素、胰岛素、血糖和胰岛素抵抗指数均显著降低(P＜0.05).结论 参苓白术散通过降低模型大鼠转氨酶与血脂水平发挥治疗NAFLD作用,其机制可能与调节瘦素、改善胰岛素抵抗有关.

Aim. This study investigated the effect and mechanism of the Chinese herbal medicine Tangshen Formula (TSF) on GI structure remodeling in the rat model of diabetes. Methods. Type 2 diabetic rats were used. Wet weight per unit length, layer thicknesses, levels of collagens I and III, nuclear factor kappa B (NF-κB), interferon-γ (IFN-γ), interleukin-6 (IL-6), transforming growth factor-β1 (TGF-β1), and Smad2/3 expression in the rat colon were measured. Results. Compared with the control group animals, wet weight and layer thicknesses of the colon increased, and expressions of collagens I and III, NF-κB, IFN-γ, IL-6, TGF-β1, and Smad2/3 increased significantly in the diabetic animals. TSF inhibited increase in colonic wet weight and layer thicknesses, downregulated expressions of collagens I and III in the mucosal layer, and downregulated expressions of NF-κB, IFN-γ, IL-6, TGF-β1, and Smad2/3 in the colon wall. Furthermore, level of expression of NF-κB was associated with those of TGF-β1 and Smad2/3. Expression of TGF-β1 was associated with the most histomorphometric parameters including colonic weight, mucosal and muscle thicknesses, and levels of collagens I and III in mucosal layer. Conclusion. TSF appears to attenuate colonic structure remodeling in type 2 diabetic rats through inhibiting the overactivated pathway of NF-κB, thus reducing expressions of TGF-β1.

The primary pathological change in postmenopausal osteoporosis (PM-OP) is bone collagen loss caused by estrogen depletion. Osteoblasts synthesize type I collagen, which composes the organic matrix of bone. Although isopsoralen stimulates osteoblastic cell proliferation and differentiation, transforming growth factor (TGF)-β1 is an important cell signaling factor for stimulating collagen synthesis. To explore the association between isopsoralen and the synthesis of collagen in vitro, the molecular and biological association between isopsoralen and TGF-β signaling was examined. (CAGA) 12-luciferase-reporter gene was used to measure TGF-β1 signaling activity. Type I collagen was detected by semiquantitative reverse transcription polymerase chain reaction, and mothers against decapentaplegic homolog 7 (Smad7) protein expression levels were analyzed by western blotting. The expression of collagen in MC3T3-E1 cells stimulated with isopsoralen was significantly upregulated compared with the control groups (P<0.05). Conversely, isopsoralen significantly decreased Smad7 protein expression compared with the control groups (P<0.05). Moreover, it was observed that isopsoralen activates the TGF-β1 signaling pathway and ultimately promotes collagen synthesis through inhibition of Smad7 protein expression. Therefore, isopsoralen is a potential target for the treatment of PM-OP.

Erchen decoction (ECD) and Linguizhugan decoction (LGZGD), both are Chinese herbal formula, have been used clinically for the treatment of nonalcoholic fatty liver disease (NAFLD). However, their therapeutic mechanisms are still unclear. Because insulin resistance (IR) is a key etiological factor in the pathology of high-fat diet- (HFD-) induced NAFLD, in this study, the protective effects of ECD and LGZGD on HFD-induced insulin resistance in rats were evaluated and their mechanisms were investigated by OGTT and Western blot. The results showed that treatment with ECD and LGZGD significantly improved insulin resistance and liver damage in rats, evidenced by supported serum aminotransferase levels and the histopathological examination. ECD and LGZGD also showed significant protective effects against HFD-induced hyperlipidemia and the inhibition of the hepatocyte proliferation by palmitate. Furthermore, supplementation of ECD and LGZGD decreased TNF-α, NF-κB, and IRS-1Ser307 phosphorylation expressions in vivo and in vitro. These results indicated that ECD and LGZGD have protective effects against HFD-induced liver IR and their underlying mechanisms involve the TNF-α and insulin pathway. These findings would be beneficial for understanding of the therapeutic effects of ECD and LGZGD in treatment of NAFLD.

目的 研究以兴趣培养为基本内容的教学模式在中西医结合学科教学与科研中的应用.方法 结合中西医结合医学的学科特点,从中医临床疗效入手,通过改变教学模式,加强理论与实践的结合,建立教师与学生的交流,个性化的指导,多种教学手段的应用,教师最后加以指导.结果 兴趣培养可以激发学生的学习兴趣,培养学生的创新意识,提高课程教学质量.结论 将兴趣培养教学模式用于教学,可以激发学生的学习兴趣,培养学生的创新意识,提高课程教学质量,并为学生从事中西医结合临床科研工作打下坚实的基础.

目的 观察益气养阴方对非酒精性脂肪性肝病(NAFLD)大鼠胰岛素抵抗(IR)的影响,探讨其作用机制.方法 采用饲喂高脂饲料建立大鼠NAFLD模型.实验大鼠随机分为正常组、模型组、阳性药组、益气养阴方组,分别给予蒸馏水、吡格列酮、益气养阴方灌胃,连续8周.进行口服葡萄糖耐量试验(OGTT),HE染色观察肝脏脂肪空泡样改变,放免法检测血清胰岛素含量,GPO-PAP法检测血清三酰甘油(TG)含量.结果 模型组大鼠肝组织出现脂肪堆积导致的空泡样病理损伤,阳性药组、益气养阴方组与模型组比较上述病理损伤明显减轻;0GTT显示口服葡萄糖2h后,模型组血糖明显高于正常组;与模型组比较,阳性药组、益气养阴方组血糖、血清胰岛素水平和TG含量明显降低(P＜0.05).结论 益气养阴方可有效防治NAFLD大鼠IR,其作用机制可能是通过抑制模型大鼠异常升高的TG和胰岛索水平,纠正机体糖脂代谢紊乱,改善其IR.

[目的]探讨经验方二陈汤与苓桂术甘汤对高脂饲料诱导大鼠非酒精性脂肪性肝炎(non-alcoholic steatohepatitis,NASH)分子作用机制.[方法]以高脂饲料喂养40只雄性SD大鼠8周,随机分为正常组、模型组、罗格列酮组、二陈汤组、苓桂术甘汤组,于第9周起分别给予罗格列酮剂量1 mg·kg-1、二陈汤4.52 g·kg-1、苓桂术甘汤组3.31 g·kg-1治疗4周.12周后将大鼠处死并观察药物对大鼠肝功能的影响,并对肝组织进行常规苏木精-伊红染色,观察病理改变;Western blot检测二陈汤与苓桂术甘汤以及两方含药血清对NASH大鼠肝组织以及经软脂酸刺激肝细胞的肿瘤坏死因子TNF-α与核转录因子NF-κB蛋白表达的影响.MTT法检测不同浓度软脂酸对大鼠肝细胞增殖的影响,以及二陈汤与苓桂术甘汤含药血清对软脂酸的拮抗作用.[结果]与模型组比较,罗格列酮和苓桂术甘汤可有效降低NASH大鼠血清ALT、AST(P＜0.05),同时改善肝脂肪变性的严重程度和降低TNF-α和NF-κB蛋白的表达(P＜0.05).与模型组比较,虽然二陈汤治疗后NASH大鼠肝组织TNF-α和NF-κB蛋白表达显著性下降(P＜0.05),但是血清ALT、AST并未显著性降低(P＞0.05),苓桂术甘汤含药血清能明显改善软脂酸对肝细胞增殖的抑制(P＜0.05).与模型组比较,二陈汤与苓桂术甘汤含药血清均能抑制软脂酸刺激的肝细胞TNF-α和NF-κB蛋白表达(P＜0.05).[结论]罗格列酮、二陈汤、苓桂术甘汤能改善大鼠肝脏脂肪变性,降低TNF-α和NF-κB蛋白表达.软脂酸可以明显抑制肝细胞增殖率,罗格列酮与苓桂术甘汤含药血清能拮抗软脂酸对肝细胞增殖的抑制.苓桂术甘汤通过抑制NF-κB蛋白表达,减少TNF-a表达,从而减轻肝脏炎性损伤,进而达到治疗NASH的作用.

Objective To investigate the effect of curcumin on the expression of nuclear transcription factor(NF-kappa B) and its inhibitory protein(Iκ-Bα) in liver cancer cells(Hepg-2) induced by TNF-α,and explore its effect on non-alcoholic steatohepatitis.Methods The cells were divided into normal group,TNF-alpha group,and different concentrations of curcumin treatment group.MTT and Western blotting were used to assay curcumin's effect on Hepg-2 proliferation activity and changes of NF-κB and Iκ-Bα's in Hepg-2.Results Compared with the normal group,TNF-α group enhanced NF-κB and Iκ-Bα expression,but the increase of Iκ-Bα had no statistical significance(P >0.05).Curcumin treatment group's NF-κB expression was significantly weakened than TNF-α group,while Iκ-Bα was significantly enhanced than that of TNF-α group.Conclusion Curcumin can antagonize NF-κB inflammatory signaling pathway activation induced by TNF-α,thus reduce the inflammatory injury of the liver cells.