Objective To investigate the inhibitory effect of Rhodiola total flavonoids on transforming growth factor (TGF)-β1-induced proliferation of cardiac fibroblasts (CFB) in the rats, and to explore its mechanisms of improving myocardial fibrosis.Methods 5 μg·L-1 TGF-β1 was used to induce the proliferation of CFB to build the cell models of myocardial fibrosis.The cultured CFB were divided into control group,model group,and low, medium,high doses (25,50 and 100 mg· L-1 )of Rhodiola total flavonoids groups.The cells were treated for 48 h,the vitalities of cells were detected by MTT,the levels of collagen proteinⅠ (ColⅠ)and collagen proteinⅢ(Col Ⅲ)in supernatant were measured by ELISA,and the activities of total superoxide dismutase (T-SOD)and glutathione peroxidase (GSH-Px)were detected,the levels of malondialdehyde (MDA)and glutathione (GSH) were also measured.Results The MTT results indicated that compared with control group,the cell vitality in model group was significantly increased (P < 0.01 ).compared with model group,the cell vitalities of CFB in Rhodiola total flavonoids groups were significantly decreased (P < 0.05 ). Compared with control group, the T-SOD activity in model group was decreased, while the MDA level was significantly increased (P <0.05);compared with model group,the T-SOD activities in 50 and 100 mg· L-1 Rhodiola total flavonoids groups were increased (P <0.01);the MDA levels in 25 and 50 mg· L-1 groups were decreased significantly (P < 0.05). Compared with control group,the GSH-Px activity and GSH level in model group were significantly decreased (P <0.01).Compared with model group,the GSH-Px activities and GSH levels in Rhodiola total flavonoids groups were increased (P <0.05).Compared with control group,the ColⅠand Col Ⅲ levels in model group were significantly increased (P <0.01);compared with model group,the ColⅠand Col Ⅲ levels in Rhodiola total flavonoids groups were significantly decreased (P <0.05).Conclusion Rhodiola total flavonoids can inhibit the proliferation of rat CFB.The development of myocardial fibrosis may be inhibited by Rhodiola total flavonoids through anti-oxidative stress pathway.

Background and purpose:In the process of gastric cancer development, cytothesis and apoptosis, and endoplasmic reticulum stress (ERS) are very important pathological processes. Glucose regulated protein 78 (GRP78) and phosphorylated form of extracellular signal-regulated protein kinase (pERK) play important roles in it. This study aimed to investigate the expression of GRP78 and pERK in gastric adenocarcinoma, chronic atrophic gastritis and superficial gastritis, and the role of GRP78 and pERK in the development of gastric adenocarcinoma. Methods:Gastric adenocarcinoma, chronic atrophic gastritis and superifcial gastritis tissues in 60 cases respectively were employed in the study. We chose 25 fresh tissue samples from each group, and the level of GRP78 and pERK mRNA in different tissues were detected by RT-PCR assay. The expressions of GRP78 and pERK in different parafifn samples were detected using immunohistochemistry assay. In addition, the relationships between GRP78 and pERK expression and age, gender, differentiation, invasion, disease stage, and lymphoid node metastasis were analyzed. Results: The expression level of GRP78 and pERK mRNA in gastric adenocarcinoma(1.26±0.18, 2.35±0.36) were significantly higher than chronic atrophic gastritis (0.89±0.25, 1.18±0.25) and superficial gastritis (0.29±0.09, 0.68±0.10, P<0.01). The positive ratio of GRP78 expression in gastric adenocarcinoma, chronic atrophic gastritis and superficial gastritis were 78.3%, 46.6%, 6.7%. The positive ratios of pERK expression were 88.3%, 43.3%, 5.0%, respectively. The GRP78 and pERK expression in different tissues were signiifcantly different (P<0.01). GRP78 and pERK expression were positively correlated with differentiation, disease stage and lymph node metastasis. There was a positive correlation between the gene and protein expression of GRP78 and pERK with a Pearson correlation value of 0.307 and 0.368, respectively. Both univariate and multivariate analysis revealed that GRP78 was related to the prognosis of gastric adenocarcinoma. Conclusion:GRP78 and pERK may play an important role in the transition of normal gastric cells to malignant cells. The expression of these two genes enhances tumor progression. Overexpression of GRP78 and pERK is significantly correlated with poor prognosis in patients with gastric adenocarcinoma. The determination of the expression of GRP78 and pERK might be helpful for the prevention, early diagnosis of gastric carcinoma. Particularly, GRP78 is valuable for the judgement of prognosis, and might be a new target for the treatment of gastric adenocarcinoma.