ABSTRACT
Objective To investigate the intervention effects of prunella vulgaris sulfated polysaccharide (PVSP) on carbon tetrachaloride(CCl4)-induced hepatic fibrosis in rat.Methods The 40% CCl4was used to induce hepatic fibrosis in rat model, then successful model rats were randomly divided into 3 groups, with 10 rats in each group, respectively, the model group(Model),the high dose PVSP group(PVSP-H:400 mg/kg)and the low dose PVSP group(PVSP-L:100 mg/kg). The blank group and solvent group were also established.The serum levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)were determined by automatic biochemical analyzer.HE staining and Sirius red staining were used to examine the degree of hepatic fibrosis.The expression levels of collagen typeⅠ(Col-Ⅰ)and α-smooth muscle actin(α-SMA)mRNA were detected by qRT-PCR.Col-Ⅰand α-SMA in hepatic tissues were detected by immunohistochemistry staining.Results There were no significant changes in serum expressions of ALT and AST and mRNA proteins of Col-Ⅰand α-SMA in liver tissues between the blank group and Solvent group.Compared with the model group,the serum levels of ALT and AST were significantly decreased in the PVSP-H and PVSP-L groups (P<0.05). HE staining and Sirius red staining showed that PVSP could significantly reduce the degree of hepatic fibrosis.The expression of Col-Ⅰand α-SMA mRNA were decreased in the PVSP-H and PVSP-L groups(P<0.05).Immunohistochemistry showed that the expressions of Col-Ⅰ and α-SMA in hepatic tissues were decreased by PVSP (P<0.05), and the effect was dose-dependent. Conclusion PVSP has a protective effect on CCl4-induced hepatic fibrosis in rats, which may be related with the inhibiting expressions of Col-Ⅰand α-SMA,reducing secretion of collagen and promoting extracellular matrix degradation.
ABSTRACT
This study was aimed to investigate the effects of blockade of Ca(2+) activated channel KCa3.1 and voltage-gated potassium channel Kv1.3 of the monocytes/macrophages on inflammatory monocyte chemotaxis. Chemotaxis assay was used to test the inflammatory Ly-6C(hi) monocyte chemotaxis caused by the monocytes/macrophages. The proliferation of monocytes/macrophages was detected by cell counting kit-8 (CCK8). Enzyme-linked immunosorbent assay (ELISA) was applied to detect the C-C motif ligand 7 (CCL7) in cultured media. The results showed that the recruitment of Ly-6C(hi) monocyte induced by monocytes/macrophages was suppressed by the potent Kv1.3 blocker Stichodactyla helianthus neurotoxin (ShK) or the specific KCa3.1 inhibitor TRAM-34. Meanwhile, the proliferation of monocytes/macrophages was significantly inhibited by ShK. The response of Ly-6C(hi) monocyte pretreated with ShK or TRAM-34 to CCL2 was declined. These results suggest that KCa3.1 and Kv1.3 may play an important role in monocytes/macrophages' proliferation and migration.