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目的:观察扶正化瘀胶囊治疗日本血吸虫病鼠早期肝纤维化的疗效并初步探讨相关机制。方法:将45只BALB/C小鼠随机分为对照组、感染组、治疗组3组,每组各15只小鼠,采用日本血吸虫尾蚴(20±1)条/只,经腹部皮肤感染BALB/C小鼠建立血吸虫病肝纤维化模型,治疗组给予扶正化瘀方4.6 g.(kg.d)-1,灌胃,qd,疗程8周。HE和Masson染色观察肝组织病理学改变,免疫组化检测转化生长因子β1(TGF-β1)、α平滑肌动蛋白(α-SMA)和血管紧张素Ⅱ1型受体(AT1R)在肝组织的表达,实时荧光定量(RT-PCR)检测检测TGF-β1、α-SMA和AT1R的mRNA水平。结果:与感染组相比,治疗组小鼠肝脏组织病理损害减轻,肝脏的胶原面积、虫卵肉芽肿结节面积分别为(0.15±0.02)mm2和(0.12±0.04)mm2,比感染组小鼠肝脏的胶原面积(0.29±0.03)mm2和虫卵肉芽肿结节面积(0.23±0.06)mm2均明显减小(P<0.05),免疫组化及RT-PCR均显示治疗组小鼠肝脏α-SMA、TGF-β1、AT1R表达显著低于感染组(P均<0.05)。结论:扶正化瘀胶囊可抑制小鼠鼠血吸虫病肝纤维化程度,其作用机制可能与其下调AT1R表达,抑制TGF-β1、α-SMA的转录,减少胶原沉积有关。
Objective: To observe the therapeutic effect of Fuzheng Huayu capsule on early liver fibrosis in schistosomiasis japonica mice and to explore the underlying mechanisms. Methods: Forty five BALB / C mice were randomly divided into control group, infection group and treatment group with 15 mice in each group. BALB / c mice were infected with cercariae of Schistosoma japonicum (20 ± 1) / C mice to establish schistosomiasis model of liver fibrosis, the treatment group given Fuzheng Huayu Fang 4.6 g. (Kg.d) -1, gavage, qd, course of treatment for 8 weeks. The liver histopathological changes were observed by HE and Masson staining. The expression of TGF-β1, α-SMA and AT1R in liver tissue were detected by immunohistochemistry The mRNA levels of TGF-β1, α-SMA and AT1R were detected by real-time fluorescence quantitative PCR (RT-PCR). Results: Compared with the infected group, the liver tissue pathological lesion in the treated group was relieved. The collagen area and the granuloma nodule area in the treated group were (0.15 ± 0.02) mm2 and (0.12 ± 0.04) mm2, respectively, which were smaller than those in the infected group Collagen area (0.29 ± 0.03) mm2 and granuloma nodule area (0.23 ± 0.06) mm2 were significantly reduced in the liver of mice (P <0.05). Immunohistochemistry and RT-PCR showed that liver α The expression of-SMA, TGF-β1 and AT1R were significantly lower than those in the infected group (all P <0.05). Conclusion: Fuzhenghuayu capsule can inhibit hepatic fibrosis in schistosomiasis mice, and its mechanism may be related to down-regulating the expression of AT1R, inhibiting the transcription of TGF-β1 and α-SMA, and reducing collagen deposition.