Objective To observe theRuangan granule on liver fibrosis in rats liver pathology change, the influence of hepatic function and hepatic fibrosis indexes, and to discusses the mechanism of its action to provide the basis for clinical prevention and treatment of liver fibrosis.Methods A total of 105 Wistar rats were randomly divided into a normal control group, a model group and a colchicines group, and Dahuang-Zhechong pill group, high-, medium- and low-doseRuangan granule groups (n=15 in each group). Liver fibrosis was induced by carbon tetrachloride and a high-cholesterol diet. After modeling, the low-, medium- and high-doseRuangan granule groups were intragastric administratedRuangan granule mixed suspension 3.6, 7.2, 14.4 g/(kg?d), respectively;Dahuang-Zhechong pill group was administrated with Dahuang-Zhechong pellets mixed suspension of 0.18 g/(kg?d); the colchicine group was intragastric administrated with colchicine mixed suspension of 0.108 mg/(kg?d); and the normal control group and the model group were intragastric administrated with the equal volume of distilled water. All rats were intragastric administrated for 8 weeks. HE staining and Masson trichromatic collagen staining were used to observe the pathological changes of liver While the change of AST, ALT, PH, TP and serum HA, LN, C-Ⅳ, PCⅢin blood serum were detected. Results Masson trichromatic collagen staining showed that, the percentage of liver collagen fiber area in rats of theRuangan granule high-dose group was significantly decreased (7.06 ± 1.18) % compared with model group (23.49 ± 1.34) %, colchicine group (11.35 ± 1.83) %, rhubarb worm pill group (15.27 ± 1.22) %,Ruangan granule medium-dose group (14.52 ± 1.75) %, and low dose group (16.08 ± 1.56) % (P<0.05 orP<0.01). Compared with model group,Ruangan granule high-dose group rats serum AST (75.86 ± 5.23 U/Lvs. 157.62 ± 24.04) U/L, the ALT (80.15 ± 5.94 U/Lvs. 160.58 ± 26.47) U/L, PH (52.58 ± 4.98μg/Lvs. 98.66 ± 6.75)μg/L significantly reduced, TP (74.19 ± 3.56 g/Lvs. 51.73 ± 5.92)g/L increased significantly (P<0.01).Ruangan granule high-dose group rats serum HA (277.22 ± 106.34 ng/mlvs. 553.19 ± 172.38 ng/ml), LN (89.82 ± 5.68 ng/mlvs. 134.25 ± 10.64 ng/ml), C-Ⅳ (47.94 ± 8.65 ng/mlvs. 84.18 ± 13.83 ng/ml), PCⅢ (16.53 ± 4.88 ng/mlvs.31.57 ± 5.35 ng/ml) decreased significantly in the model group (P<0.01).ConclusionRuangan granule has obvious effects for resisting liver fibrosis.

Objective To investigate the effects of Ruangan granule on transforming growth factor-β1(TGF-β1)/Smads signaling pathway in liver fibrosis in rats. Methods A total of 105 Wistar rats were randomly divided into normal control group, model group and colchicine, Dahuang-Zhechong pill group, high-, medium- and low-dose Ruangan granule groups (n=15 in each group). Liver fibrosis was induced by carbon tetrachloride and a high-cholesterol diet. After modeling, the low-, medium- and high-dose Ruangan granule groups were intragastric administrated Ruangan granule mixed suspension 3.6, 7.2, 14.4 g/(kg?d), respectively;Dahuang-Zhechong pill group was administrated with Dahuang-Zhechong pellets mixed suspension of 0.18 g/(kg?d);the colchicine group was intragastric administrated with colchicine mixed suspension of 0.108 mg/(kg?d);and the normal control group and the model group were intragastric administrated with the equal volume of distilled water. All rats were intragastric administrated for 8 weeks. The expressions of TGF-β1, Smad3 and Smad7 proteins in the liver tissue were detected with immunohistochemical staining method. The expressions of TGF-β1, Smad3, Smad7 mRNAs in the liver tussue were detected by RT-PCR. Results The expressions of TGF-β1 (2.59 ± 0.99 vs. 0.43 ± 0.21) and Smad3 (2.56 ± 0.67 vs. 0.41 ± 0.18) proteins and TGF-β1 mRNA (2.25 ± 0.21 vs. 0.71 ± 0.09) and Smad3 (2.34 ± 0.03 vs. 0.78 ± 0.12) mRNAs in the model group were significantly increased than those in the normal control group (all P<0.01). Compared with the model group, the expressions of TGF-β1 (1.12 ± 0.27 vs. 2.59 ± 0.99) and Smad3 (1.05 ± 0.34 vs. 2.56 ± 0.67) proteins in the high-dose Ruangan granule group decreased significantly, the expression of Smad7 increased significantly (2.33 ± 0.62 vs. 0.36 ± 0.18), and the expressions of TGF-β1 (1.09 ± 0.11 vs. 2.25 ± 0.21) and Smad3 (1.10 ± 0.02 vs. 2.34 ± 0.03) mRNAs decreased significantly, the expression of smad7 mRNA (1.18 ± 0.13 vs. 0.38 ± 0.11) increased significantly (P<0.05). Conclusions Ruangan granule can regulate the TGF-β1/Smads signaling pathway via down-regulation of TGF-β1, Smad3 and up-regulation of Smad7 in liver fibrosis in rats.

This article introduced Professor Xie Jingri's clinical experience in explaining the etiology,pathogenesis and treatment of cirrhotic ascites based on the theory of collateral disease.Professor Xie Jingri believes that cirrhotic ascites is mostly the syndrome of deficiency in origin and excess in superficiality,and the mixture of deficiency and excess.Among them,the deficiency of collaterals is the root of the pathogenesis of cirrhotic ascites,and qi stagnation,water dampness,blood stasis and other pathogenic factors blocking collaterals are its superficiality.The treatment should be based on the basic principles of tonifying deficiency and dredging collaterals,promoting qi and dredging collaterals,removing dampness and dredging collaterals,and promoting blood circulation and dredging collaterals.One medical case about liver cirrhosis ascites of qi stagnation and collateral obstruction type was attached in this article.The treatment should be promoting qi and dredging collaterals,with confirmed clinical efficacy.

Traditional Chinese Medicine (TCM) shows unique advantages in the field of adjuvant treatment of gastric cancer. The main mechanism of TCM in improving gastric cancer includes regulating cell proliferation and apoptosis, reversing cell resistance, reducing the ability of invasion and metastasis and epithelial-mesenchymal transformation, regulating immune function, inhibiting neovascularization, regulating autophagy exosome, and ferroptosis.