目的 研究清肠温中方调控DSS诱导溃疡性结肠炎(UC)大鼠Th17/Treg免疫平衡及肠黏膜屏障的作用机制.方法 24只SPF级雄性SD大鼠,按体质量依照随机数字表将其随机分为空白组、模型组、清肠温中方组.空白组自由饮用去离子水,同时予去离子水灌胃;模型组和清肠温中方组自由饮用4.5％ DSS溶液制备UC模型,同时模型组给予去离子水,清肠温中方组予清肠温中方灌胃.7d后麻醉大鼠后取血及结肠组织,应用Real time-PCR法检测结肠miR-675-5p、VDR mRNA、RORγt mRNA、Foxp3 mRNA的表达,ELISA法检测血清IL-10、IL-17的表达,免疫组织化学法检测ZO-1、Occludin的蛋白表达及分布.结果 与空白组比较,DSS诱导的UC大鼠结肠miR-675-5p、RORγt mRNA及血清IL-17的表达较空白组明显升高(P＜ 0.05或P＜0.01),VDR mRNA、Foxp3 mRNA、ZO-1、Occludin、血清IL-10的表达较空白组明显降低(P＜ 0.05或P＜0.01);清肠温中方干预后,大鼠结肠miR-675-5p、RORγt mRNA、血清IL-17的表达较模型组明显降低(P＜0.05),VDR mRNA、Foxp3 mRNA、ZO-1、Occludin、血清IL-10的表达较模型组明显升高(P＜ 0.05或P＜0.01).结论 清肠温中方可能通过降低miR-675-5p的表达,靶向调控VDR信号通路,从而调控溃疡性结肠炎Th17/Treg免疫平衡、修复肠黏膜屏障损伤,达到治疗UC的目的.

目的:观察苓桂术甘汤与茵陈蒿汤合方(茵陈苓桂术甘汤)对非酒精性脂肪性肝炎大鼠细胞自噬的影响,初步探讨合方对非酒精性脂肪性肝炎大鼠的作用机制.方法:将SPF级SD大鼠随机分为正常对照组、模型组、茵陈苓桂术甘汤组、苓桂术甘汤组、茵陈蒿汤组,采用高脂饲料法建立NASH模型;高脂饲料饲养8周并同时给药,Western Blot法测定LC3Ⅱ、LC3Ⅰ表达量,Western Blot与RT-PCR法测定肝脏p62、ATG5蛋白与基因表达水平.结果:给药后,模型组大鼠肝脏ATG5表达量、LC3Ⅱ/LC3Ⅰ比值下降,p62表达量上升(P＜0.05);与模型组比较,各给药组大鼠肝脏ATG5表达量、LC3Ⅱ/LC3Ⅰ比值有不同程度上升,p62表达量下降(P ＜0.05,P＜0.01).结论:茵陈苓桂术甘汤可能通过激活细胞自噬,从而达到改善氧化应激,防治NASH的目的.

Objective:To observe the effects of HWJNF on receptors of 5-hydroxytryptamine in rats with non-erosive gastroesophageal reflux disease.Methods:The SD rats were randomly divided into control group,model group,omeprazole group and the high,medium and low HWJNF groups.Except for the control group,the rats of all the other groups received basalovalbumin-sensitization combined with intra-esophageal mucosal acid exposure to establish NERD models.Then,the treatment was given for 2 weeks.The comparative observation was carried out on the expression of 5-HT3R and 5-HT4R with the methods of Western Blot and RT-PCR.Results:The omeprazole group and the high,medium and low HWJNF groups showed lower expressive levels of 5-HT3R in the esophageal than the model group (P＜0.05).However,the levels of 5-HT4R didn't show statistical differences among the omeprazole group and the high,medium and low HWJNF groups and model groups (P＞0.05);The middle and low HW.JNF groups showed lower expressive levels of 5-HT3RmRNA in the esophageal than the model group (P＜0.01 or P＜0.05).However,there was no difference among the omeprazole group and the high,medium and low HWJNF groups and model groups in 5-HT4RmRNA (P＞0.05).Conclusion:HWJNF may regulate esophagus-visceral sensitivity to treat NERD according reducing 5-HT3R expression in the esophageal.

Objective To explore the effects of Gegen Qinlian decoction on NLRP3 in experimental non-alcoholic steatohepatitis (NASH). Methods 36 rats were randomly divided into 6 groups:the chow group,the model group,the high-dose Gegen Qinlian decoction group, the middle-dose Gegen Qinlian decoction group, the low-dose Gegen Qinlian decoction group and glutamine group. Treatments with saline, Gegen Qinlian decoctions and glutamine were given as the model establishment began. Liver tissue and small intestine tissue were harvested after 8 weeks treatment and NLRP3 was detected by Western-blot and RT-PCR. Results In liver, compared with chow group, the protein and mRNA levels of P10 in model group were increased. Gegen Qinlian decoction attenuated the elevated P10 protein (P<0.05). In small intestine tissue, compared with chow group, the protein levels of P10 in model group were increased. Both Gegen Qinlian decoction and glutamine group attenuated the elevated P10 protein (P<0.05). Conclusion The data suggested that Gegen Qinlian decoction could decrease the activation of NLRP3 both in liver and gut in experimental NASH model.

目的 观察温中健脾、清热燥湿法对TNBS/无水乙醇诱导的寒热错杂证溃疡性结肠炎(UC)大鼠及Occludin蛋白的作用影响并探讨其作用机制.方法 70只雄性SD大鼠随机分为7组,除空白组外,其余均用5％ TNBS/无水乙醇保留灌肠3d复制寒热错杂证UC大鼠模型,造模后分别用蒸馏水,清肠温中浸膏高、中、低剂量,美沙拉秦缓释颗粒和乌梅丸颗粒剂灌胃干预10d,记录大鼠疾病活动指数、结肠黏膜损伤指数(CM-DI),观察结肠组织病理改变,免疫组化染色观察Occludin蛋白表达.结果 与空白组比较:模型组大鼠体质量明显减轻(P＜ 0.01);便潜血、便质、CMDI、结肠组织病理评分明显升高(P＜0.01);结肠Occludin蛋白表达明显减少(P＜0.01).与模型组比较:中药中剂量、乌梅丸和美沙拉秦组体质量均增加((P＜ 0.05或P＜0.01);中药中剂量和美沙拉秦组便潜血和便质评分下降(P＜0.05),病理组织评分明显降低(P＜0.01),Occludin蛋白表达明显增加(P＜0.01);美沙拉秦组CMDI评分降低(P＜0.05),中药组评分下降但差异尚无统计学意义(P＞0.05).结论 温中健脾、清热燥湿法可以减轻TNBS/无水乙醇诱导的寒热错杂证UC大鼠疾病程度,改善体质量、便潜血和便质,减轻结肠黏膜损伤,修复结肠黏膜组织病变并增加Occludin蛋白表达,提高肠上皮细胞间紧密连接完整性,从而起到治疗UC的效果.

BACKGROUND:Ulcerative colitis (UC) is a kind of complex immune disease, the pathogenesis of which remains elusive. Destruction of the intestinal barrier, extreme inflammation, oxidative stress, and apoptosis might play key roles in the development of UC. In previous studies, we observed that Qingchang Wenzhong granule (QCWZG) had the exact effect on the remission of UC in the clinic; however, the underlying mechanism has not been identified. This study aimed to reveal the effects of QCWZG on the intestinal physical barrier and the interactive network of inflammation, oxidative stress, and apoptosis in rats with dextran sulfate sodium (DSS)-induced colitis.METHODS:Sixty rats were randomly divided into six groups: blank group, model group, high/mild/low-dose QCWZG groups, and mesalazine group. The rats in the experimental group drank 4% DSS for 7 days and 1% DSS for the subsequent 7 days. Different medications or distilled water was supplied by intragastric administration for 7 days. The levels of colitis and indices related to inflammation, oxidative stress, and apoptosis were assessed.RESULTS:Compared with the model group, the QCWZG group (P < 0.05) demonstrated attenuated disease activity index, colonic mucosa disease index, histological lesions, and colonic weights; lower levels of inflammatory substances, such as interleukin (IL)-1α, IL-6, tumor necrosis factor-α, and myeloperoxidase; lower levels of malondialdehyde; and increased levels of superoxide dismutase and glutathione peroxidase. The QCWZG group also demonstrated elevated expression of Bcl-2 and occluding but downregulated db expression of Bax and caspase 3 in the colon.CONCLUSION:QCWZG could relieve rats with DSS-induced colitis from UC symptoms by improving the intestinal physical barrier, which resists the interactive network of inflammation, oxidative stress, apoptosis, and their overactivated interactions.

Objective: To study the effects of intestine-clearing middle energizer-warming prescription on inflammatory factors of TNBS-induced ulcerative colitis(UC)rat model.Methods: Seventy male SD rats were ran-domized into seven groups,besides the blank group,other rats accepted retention enema of 5％TNBS/absolute ethyl alcohol to duplicate UC models,after modeling,the rats were intervened with distilled water,high,moderate and low doses of intestine-clearing middle energizer-warming prescription,mesalazine sustained release granules and the granules of W uMei pills for ten days respectively,disease activity index(DAI)and general state of the rats were recorded,the contents of IL-13,IFN-γ,IL-6 and TNF-α in the serum were detected by enzyme linked immunosor-bent assay(ELISA),and the expressions of NF-κB p50 protein in the intestinal mucosa were observed by immuno-histochemical staining.Results: After drug intervention,compared with the blank group,DAI of the rats in the model group increased obviously(P＜0.01),the contents of IFN-γ,IL-6 and TNF-α in the serum evaluated notably(P＜0.01),the contents of IL-13 lowered remarkably(P＜0.01); the expressions of NF-κB p50 protein in the intestinal mucosa up regulated(P＜0.01).Compared with different indexes of the model group,these in moderate dose group of intes-tine-clearing middle energizer-warming prescription and mesalazine group improved(P＜0.05).Conclusion: Intes-tine-clearing middle energizer-warming prescription could treat UC rats by reducing the inflammatory factors of UC rats and increasing the expressions of inflammatory factors.

[目的]探讨茵陈二陈汤对非酒精性脂肪性肝炎(NASH)模型细胞内IRS-1ser307、PKBser473蛋白表达的影响;[方法]采用游离脂肪酸500 umol/L(棕榈酸:油酸摩尔比例为1∶2)刺激干预HepG2细胞,干预24 h建立细胞模型,采用茵陈二陈汤含药血清干预模型细胞,干预治疗24 h;选用罗格列酮、多烯磷脂酰胆碱含药血清作为治疗观察对照;Western Blot检测茵陈二陈汤对模型细胞内IRS-per307、PKBser473蛋白表达及IRS-1ser307/IRS-1、PKBser473/PKB的影响.与空白组相比,游离脂肪酸刺激24 h后,模型细胞内IRS-1ser307蛋白表达及IRS-1ser307/IRS-1水平明显升高,PKBser473蛋白及PKBser473/PKB水平显著下降;与模型组相比,茵陈二陈汤干预24 h后,模型细胞内IRS-1ser307蛋白表达(P＜0.01)及IRS-1ser307/IRS-1水平(P＜0.01)显著降低,PKBser473蛋白(P＜0.05)及PKBser473/PKB水平(P＜0.05)明显升高,且差异具有统计学意义.[结论]①茵陈二陈汤可通过调节IRS-1ser307、PKBser473蛋白表达,降低肝细胞IRS-1蛋白活化水平,促进PKB磷酸化,从而达到干预治疗作用;②茵陈二陈汤对IRS-1ser307、PKBser473蛋白的影响作用与罗格列酮及多烯磷脂酰胆碱效果相近.

Objective:To study the protective effect of Compound Kuijiekang Enema on colonic mucosa of rats with ulcerative colitis gravis induced by DSS. Methods:The rats were randomly divided into 6 groups:the nor-mal group,the model group,low dose group (787.5 mg/kg),middle dose group (1575 mg/kg),high dose group (3150 mg/kg)and mesalazine group(5 mL/kg).Except the normal group,the other groups drank 4.5% of the DSS freely for seven days to prepare the ulcerative colitis model. The treatment groups were given the corresponding drugs for enema intervention. The weight of rats was daily weighed;fecal occult blood was detected,as well as disease activity index (DAI). After the intervention,the rats were killed,and the colon tissues were taken. The pathological damage and the histopathology (HS) of the colon were observed,and the activity of myeloperoxidase (MpO) was detected by chemical colorimetry. Results:Compared with the normal group,hair color,activity,oc-cult blood,stool and other general condition were poor in DSS-induced UC rats;the body mass decreased obvi-ously;DAI index was the largest,and the pathological damage was obvious. The HS score was the heaviest,and the activity of MpO was higher than that of the normal group(P<0.01).After 7 days of enema intervention,all the treatment groups had different degrees of improvement,and DAI index,HS score and MpO activity were decreased significantly (P<0.01).Conclusion:Compound Kuijiekang Enema has a good therapeutic effect on colitis gravis in rats induced by DSS by improving the clinical symptoms such as abdominal pain,diarrhea and colitis,reducing infiltration of inflammatory cells and protecting the colonic mucosa.

流行病学研究调查显示非酒精性脂肪性肝炎 (NAFLD) 近年来发病率呈上升趋势[1], 目前不少西药在临床中已观察到可以改善NAFLD, 但治疗NAFLD疗效并不理想, 并且长期服用安全性等问题仍处于探索阶段[2-4].而中医对于NAFLD的治疗具有独特的理论和雄厚的临床基础, 在NAFLD的临床治疗中具有丰富的临床经验.随着西医对NAFLD的认识的深入, 中医学对NAFLD病因和治疗也不断有新的认识.目前, 中医界对NAFLD病因病机的认识已渐趋一致, 但具体的治疗则依学者经验不同, 呈现出多样化的特点.中医在改善肝功能、调节脂质代谢上具有比较明显的疗效和优势, 尤其是在"整体观念"和"辨证论治"的指导下, 在改善患者的生存质量上具有较为明显的优势.

Yinchen Linggui Zhugan Decoction (YCLGZGD) is the combination of Linggui Zhugan (LGZGD) and Yinchenhao (YCHD) decoctions, two famous traditional Chinese medicine prescriptions. In previous studies, we found that Yinchen Linggui Zhugan Decoction (YCLGZGD) could regulate lipid metabolism disorder and attenuate inflammation in pathological process of nonalcoholic fatty liver disease (NAFLD). However, the exact underlying mechanism remains unknown. The aim of this study was to explore the effect of Yinchen Linggui Zhugan Decoction on experimental NAFLD and its mechanism in rats with high-fat diet (HFD) which was established by 8-week administration of HFD. YCLGZGD, LGZGD, and YCHD were administered daily for 4 weeks, after which the rats were euthanized. The level of blood lipid, liver enzymes, H&E, and Oil Red O staining were determined to evaluate NAFLD severity. Western blotting and real-time polymerase chain reaction were, respectively, used to determine hepatic protein and gene expression of Keap1, Nrf2, NQO1, and HO-1. Oral YCLGZGD ameliorated HFD-induced NAFLD. Furthermore, YCLGZGD increased the protein and gene expression of Nrf2, NQO1, and HO-1 without changing Keap1. Overall, these results suggest that YCLGZGD ameliorates HFD-induced NAFLD in rats by upregulating the Nrf2/ARE signaling pathway.

This paper was aimed to study the effect of Qing-Chang Wen-Zhong (QCWZ) decoction on interferon gamma induced protein 10 (IP10) in colon tissues of rats with ulcerative colitis (UC).The UC model was induced using 4.5％ DSS added to distilled water for 7 days.At the same time,low-,medium-and high-dose of QCWZ decoction and mesalazine was given by gavage route daily.Then,the rats were killed and the colon tissues were taken.Expression level of interleukin-1 alpha (IL-1α),IL-1β,IL-6,tumor necrosis factor alpha (TNF-α) and interferon gamma (INF-γ) in colon were detected by Elisa assay.The expression and distribution of IP10 protein were detected by immunohistochemistry (IHC).The results showed that compared with the normal group,inflammatory factors (IL-1α,IL-1β,IL-6,TNF-α,INF-γ) and IP10 expression level in DSS-induced UC rats were significantly increased.After 7 days of intervention,inflammatory factors (IL-1α,IL-1β,IL-6,TNF-α,INF-γ) and IP10 decreased significantly (p＜0.01,p＜0.05).It was concluded that QCWZ decoction may down-regulate the expression of IP 10 and inflammatory factors (IL-1α,IL-1β,IL-6,TNF-α,INF-γ),and then inhibit intestinal inflammation and repair intestinal mucosal damage,so as to achieve the purpose of UC treatment.

Objective:To explore the changes of NGF/PLC-γ/TRPV1 signaling pathway in rat models with IBS-D and the intervention effect of Tongxie Anchang Decoction.Methods:The model of IBS-D was made by intracolonic instillation of acetic acid,balloon rectal dilatation and tail clamping stimulation.After modeling,60 SD rats were randomly divided into the model group,the intervention groups (low-dosage,middle-dosage,and high-dosage),Dicetel group and the blank group.Abdominal withdrawal reflex (AWR) scores of rats were observed before and after treatment,as well as Bristol grading score and water content of feces.Western Blot was used to detect the expression of NGF,PLC-γand TRPV1 in colon,and the mRNA expressions of NGF,PLC-γ,and TRPV1 in colon were detected by Real-Time and PCR.Results:The visceral sensitivity threshold of the model group was lower than that of the blank group (P＜0.05 or P＜0.01).Bristol score and water content were significantly increased (P＜ 0.01).After treatment,the visceral sensitivity threshold increased in the intervention groups (low-dosage,middle-dosage,and high-dosage) and Dicetel group (P ＜ 0.05 or P ＜ 0.01).Bristol grading score and water content decrease (P ＜ 0.01).Protein expression of colon N GF,PLC-γ and TRPV1 decreased (P ＜ 0.05 or P＜0.01);mRNA expression of PLC-γand TRPV1 decreased (P＜0.01).Conclusion:Tongxie Anchang Decoction can reduce visceral hypersensitivity of IBS-D rats.The mechanism may be achieved by downregulating the protein expression of colon NGF,PLC-γ and TRPV1,decreasing the mRNA expression of colon PLC-γand TRPV1,and upregulating visceral sensitivity.

Ulcerative colitis (UC) is a chronic, nonspecific, inflammatory disease for which an effective treatment is lacking. Our previous study found that Qingchang Wenzhong Decoction (QCWZD) can significantly improve the clinical symptoms of UC and ameliorate dextran sulphate sodium- (DSS-) induced ulcerative colitis in rats by downregulating the IP10/CXCR3 axis–mediated inflammatory response. The purpose of the present study was to further explore the mechanism of QCWZD for UC in rats models, which were established by 7-day administration of 4.5% dextran sulphate sodium solution. QCWZD was administered daily for 7 days; then we determined the serum macrophage-stimulating protein concentration (MSP) and recepteur d’origine nantais (RON) expression and its downstream proteins (protein kinase B [Akt], phosphorylated [p] Akt, occludin, zona occluden- [ZO-] 1, and claudin-2) in colon tissue using Western blotting and quantitative polymerase chain reaction. In DSS-induced UC, QCWZD significantly alleviated colitis-associated inflammation, upregulated serum MSP expression and RON expression in the colon, reduced the pAkt levels, promoted colonic occluding and ZO-1 expression, and depressed claudin-2 expression. In conclusion, the MSP/RON signalling pathway plays an important role in the pathogenesis of UC by involving the inflammatory response and improving intestinal barrier function. QCWZD appears to attenuate DSS-induced UC in rats by upregulating the MSP/RON signalling pathway.

[Objective]To evaluate the effect of Astragalus,Panax notoginseng and their compatibility on apoptosis and proliferation of the gastric mucosa in rats with chronic atrophic gastritis(CAG).[Methods] CAG model was established by implantation of a pyloric spring and intragastic administration of hot starch paste with high-salt.The model rats were randomly divided into model group,sham operation group,folic acid group,Astragalus group,Panax notoginseng group and Astragalus plus Panax notoginseng group.The normal wistar rats were taken as control group.In the 8 weeks therapeutic phase,the control,sham operation and model groups were given normal saline 2 mL daily.The Astragalus group was given water decoction of Astragalus containing crude drug 3.5 g/(kg · d).The Panax notoginseng group was infused with Panax notoginseng powder containing crude drug 0.7 g/(kg · d).The Astragalus plus Panax notoginseng group was given both Panax notoginseng powder and Astragalus water decoction.TUNEL was used to evaluate gastric mucosal cell apoptosis index and liquid phase chip to evaluate fas,fasl,EGF and TGF-β expression,the protein expression level of PCNA was detected by immunological histological chemistry assay.[Results]Compared with the control group,the apoptosis index in the model group decreased significantly(P＜0.01).The expression of PCNA was significantly increased(P＜0.01),serum levels of fas and fas-L increased significantly (P＜ 0.01),serum EGF level was significantly reduced (P ＜ 0.05).Compared with the model group,the level of fas of all the treatment groups was reduced(P＜0.05,P＜0.01).The Astragalus group and Astragalus plus Panax notoginseng group reduced the level of fas-L significantly(P＜ 0.05).[Conclusion]Astragalus,Panax notoginseng and their compatibility can effectively protect the gastric mucosal of CAG rats by improving the level of proliferation and apoptosis of gastric mucosal cells.

ErChen and YinChen decoction (ECYCD) is an effective traditional Chinese medicine and has been widely used in traditional Chinese medicine to treat nonalcoholic steatohepatitis (NASH), with good curative effects. However, the specific mechanisms underlying these effects are unclear. In this study, we determined the efficacy of ECYCD in a high-fat diet-induced NASH rat model, established by 8-week administration of a high-fat diet. ECYCD was administered daily for 4 weeks, after which the rats were euthanized. The results demonstrated that ECYCD ameliorated high-fat diet-induced NASH, as evidenced by decreased liver indexes, reduced hepatic lipid deposition and liver injury, lower serum biochemistry markers (including low-density lipoprotein), and reduced HOMA-IR scores. Moreover, levels of free fatty acids, tumor necrosis factor, and malondialdehyde were decreased, whereas glutathione was increased in the liver. Serum high-density lipoprotein was also increased in the liver, and ECYCD regulated the c-Jun N-terminal kinase 1 (JNK1) signaling pathway by decreasing the levels of JNK1 protein, JNK1 mRNA, activator protein-(AP-) 1 protein, AP-1 mRNA, and phospho-insulin receptor substrate-(IRS-) 1(ser307) and increasing phopsho-PKBser473 levels. These results suggested that ECYCD could ameliorate high-fat diet-induced NASH in rats through JNK1 signaling. ECYCD may be a safe therapeutic option for the treatment of NASH.

Objective:To observe the effects of HWJNF on 5-hydroxytryptamine and receptors of non-erosive gastroesophageal reflux disease rats and to investigate mechanism of HWJNF.Methods:The SD rats were randomly divided into 6 groups,control group,model group,omeprazole group and the high,medium and low groups of HWJNF;Except the control group,the rats of all the other groups received hasal ovalbumin-sensitization combined with intra-esophageal mucosal acid exposure for making NERD models.The treatment was given for 2 weeks.The comparative observation was carried out on the changes of pathologic structure and the expression of 5-HT,5-HT3R,5-HT4R via the methods of Elisa,HE and immunohistochemical staining.Results:The middle and low groups of HWJNF and omeprazole group showed lower expressive levels of 5-HT in the serum than the model group (P＜0.05),besides,the middle group of HWJNF and omeprazole group showed lower expressive levels of 5-HT in the esophageal than the model group (P＜0.05).The high and medium groups of HWJNF showed lower levels of 5-HT3R than the model group (P＜0.05).Conclusion:HWJNF can reduce the levels of 5-HT in serum and esophageal,the mechanism of which may be in relation with decreasing the level of 5-HT3R in the esophageal.

Objective:To observe the effects of combined prescription of Linggui Zhugan Tang (LGZGT) and Yinchenhao Tang (YCHT) on Nrf2/ARE signaling pathway in rats with non-alcoholic steatohepatitis (NASH) from the perspective of oxidative stress,and investigate its mechanism for treating non-alcoholic steatohepatitis.Method:SPF grade SD rats were randomly divided into normal control group,model group,sulforaphane group (0.5 mg·kg-1),LGZGT group (3.465 g·kg-1),YCHT group (3.465 g·kg-1) and LGZGT + YCHT combination group (6.93 g·kg-1).High-fat diet was given to establish NASH models,and the treatment was given at the same time for 8 weeks.Then the serum was harvested separately to detect the levels of alanine aminotransferase (ALT),aspartate aminotransferase (AST),total cholesterol (TC),triglyceride (TG),highdensity lipoprotein (HDL-C),and low density lipoprotein (LDL-C);part liver tissues were taken for HE staining;Western blot and reverse transcription PCR were used respectively to detect the protein and mRNA expression levels of Kelch-like ECH-associated protein 1 (Keap1),nuclear factor E2-related factor 2 (Nrf2),quinone oxidoreductase-1 (NQO1),and heme oxygenase-1 (HO-1).Result:As compared with normal control group,the levels of TC,TG,HDL-C and LDL-C in blood lipid and ALT,AST levels in serum were increased;liver fat became obvious;the expression level of Keap1 in liver was decreased;and,Nrf2,NQO1,HO-1 protein and mRNA expression levels were increased in the model group (P ＜ 0.05).As compared with the model group,the levels of TC,TG,HDL-C and LDL-C in blood lipid and ALT,AST levels in serum were decreased in various treatment groups,liver pathology was also improved to some extent;and Nrf2,NQO1,HO-1 protein and mRNA expression levels were increased in treatment groups (P ＜ 0.01,P ＜ 0.05) except YCHT group.However,the levels of Keap1 didn't show obvious differences among the treatment groups.Conclusion:LGZGT and its combination formula may improve oxidative stress to prevent and treat NASH via activating Nrf2/ARE signaling pathway in the liver.

[Objective]We aimed to research whether YCECD had an effect on JNK1、AP-1 prteins in NASH model cell.[Methods]The 500 μmol/L free fatty acids(palmitic acid and oleic acid with the molar ratio of 1 ∶ 2)stimulated HepG2 cells for 24 hours to establish NASH model cell.We intervened NASH model cell with YCECD containing serum for 24 hours,Rosiglitazone and Polyenylphosphatidylcholine containing serum were used as the positive control.CCK-8 method was used to select the perfect drug containing serum concentration.We detected the effect of YCECD containing serum on JNK1,and AP-1 prteins in NASH model cell with western blot.[Results]compared with the control group,JNK1,and AP-1 protein levels were increased in model cells after 24 hours stimulation.Compared with model group,YCECD significantly inhibited the increases of JNK1,and AP-1 protein levels after 24 hours intervention.[Conclusion]①YCECD adjusted JNK1 and AP-1 protein expression in NASH model cell by decreasing JNK1,and AP-1 levels,and achieved the curative effect.②YCECD had a similar effect with Rosiglitazone and Polyenylphosphatidylcholine on JNK1 and AP-1 protein levels.

Qingchang Wenzhong Decoction (QCWZD) is an effective traditional Chinese medicine prescription. Our previous studies have shown that QCWZD has significant efficacy in patients with mild-to-moderate ulcerative colitis (UC) and in colonic mucosa repair in UC rat models. However, the exact underlying mechanism remains unknown. Thus, this study was conducted to determine QCWZD's efficacy and mechanism in dextran sulphate sodium- (DSS-) induced UC rat models, which were established by 7-day administration of 4.5% DSS solution. QCWZD was administered daily for 7 days, after which the rats were euthanized. Disease activity index (DAI), histological score (HS), and myeloperoxidase (MPO) level were determined to evaluate UC severity. Serum interferon gamma-induced protein 10 (IP10) levels were determined using ELISA kits. Western blotting and real-time polymerase chain reaction were, respectively, used to determine colonic protein and gene expression of IP10, chemokine (cys-x-cys motif) receptor (CXCR)3, and nuclear factor- (NF-) κB p65. Intragastric QCWZD administration ameliorated DSS-induced UC, as evidenced by decreased DAI, HS, and MPO levels. Furthermore, QCWZD decreased the protein and gene expression of IP10, CXCR3, and NF-κB p65. Overall, these results suggest that QCWZD ameliorates DSS-induced UC in rats by downregulating the IP10/CXCR3 axis-mediated inflammatory response and may be a novel UC therapy.