Antihepatofibrotic Effects of Aqueous Extract of Prunella vulgaris on Carbon Tetrachloride-Induced Hepatic Fibrosis in Rats

Abstract

Prunella vulgaris has been widely used in the folk medicine of Northeastern Asian countries for the treatment of acute liver injury and infectious hepatitis. In the present study, the protective effect of aqueous extract from P. vulgaris was investigated on carbon tetrachloride-induced hepatic fibrosis in vivo. Our data showed that the administration of aqueous extract from P. vulgaris at doses of 50, 100, and 200 mg/kg significantly reduced the elevated serum levels of alanine aminotransferase, aspartate aminotransferase, type III precollagen, and hyaluronic acid in rats with hepatic fibrosis. In addition, aqueous extract from P. vulgaris also reduced the incidence of liver lesions and the formation of fibrous septa, and remarkably decreased the serum levels of inflammatory cytokines, platelet derived growth factor, interleukin-4, interleukin-8, and tumor necrosis factor alpha. Furthermore, aqueous extract from P. vulgaris significantly inhibited the activation of hepatic stellate cells by regulating the expression of α smooth muscle actin, transforming growth factor β 1, and smad2 and also decreased the deposition of extracellular matrix proteins via regulating the expressions of tissue inhibitor of metalloproteinase-1, matrix metalloproteinase-2,-13. Real-time polymerase chain reaction further revealed that post-treatment with aqueous extract from P. vulgaris decreased the elevated levels of miR-34a and miR-199a-5p in hepatic fibrosis rats. These results demonstrated that aqueous extract from P. vulgaris alleviates carbon tetrachloride-induced hepatic fibrosis by inhibiting the activation of hepatic stellate cells, promoting collagenolysis and regulating fibrosis-related microRNAs.

Effects of a Long-Term Administration of Aqueous Extract of Prunella vulgaris L. on Survival, Spontaneous Thyroid Carcinoma and Neoplastic C-cell Hyperplasia in Rats

“…PV consumption did not lead to remarkably changes in survival, body weight and majority of metabolic indicators (ATL, TP, ALB, BUN, CREA, glucose, TG and TC) in both female and male rats. Meanwhile, a signi cant decrease in AST was detected only in male rats fed high dose of PV, which tted well with ndings of Qu et al [16] suggesting that PV has the potential to protect liver function, and this effect may differ by sex. In disagreement with previous animal studies [17][18][19], the hypoglycemic, hypolipidemic and renal-protective functions of PV were not observed in the present study.…”

Exogenous Plant gma-miR-159a, Identified by miRNA Library Functional Screening, Ameliorated Hepatic Stellate Cell Activation and Inflammation via Inhibiting GSK-3β-Mediated Pathways

“…The mice (4 weeks old) were intraperitoneally injected with 0.1 mL of peanut oil containing 20% CCl 4 twice a week for 6 weeks to induce hepatic fibrosis. 22 , 23 The mice with hepatic fibrosis were randomly divided into a model group, a miR159a-treated group, and a silymarin-treated group (as the positive control group). Each group had eight mice.…”

“…Histopathological features were analyzed in the same manner as in our previous study. 22 Histological changes in each liver tissue were individually calculated in three aspects, namely, steatosis, fibrosis, and inflammation, and then appraised by counting the scores of each item.…”

MicroRNA134 Mediated Upregulation of JNK and Downregulation of NFkB Signalings Are Critically Involved in Dieckol Induced Antihepatic Fibrosis

“…Liver fibrosis is a liver disease with excessive accumulation of extracellular matrix induced by chronic liver inflammation by alcohol abuse, metabolic diseases, viral hepatitis, cholestatic liver diseases, and autoimmune diseases eventually leading to liver cirrhosis. − Also, it was well documented that the activation of hepatic stellate cells (HSCs) plays a pivotal role during the initiation and development of liver fibrosis. , Activated HSCs by various kinds of pathologic factors are fibrogenic and proliferative, and they subsequently accumulate ECM, while HSCs are normally quiescent. , Thus, recently, several research projects were conducted targeting HSC activation with natural compounds such as oridonin, galangin, puerarin, ligustrazine, and paeoniflorin and herbal medicines such as Prunella vulgaris and Sho-saiko-to, since HSC activation is an important event in fatty livers.…”