Abstract
Herbal medicines harbor essential therapeutic agents for the treatment of cholestasis. In this study, we have assessed the anticholestatic potential of Stachys pilifera Benth's (SPB's) hydroalcoholic extract encapsulated into liposomes using bile duct ligation- (BDL-) induced hepatic cholestasis in rats. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), malondialdehyde (MDA), total thiol (T-SH) content, protein carbonyl (PCO), total bilirubin (TBIL), albumin (ALB), and nitric oxide (NO) metabolite levels were measured in either liver tissue or plasma to assess liver damage. Moreover, expression of proinflammatory cytokines (IL-1β and TNF-α) and liver fibrosis markers (TGF-β and SM-α) which are driving forces of many liver disorders was also determined. The activity of AST, ALT, and ALP was significantly enhanced in the BDL group in comparison to the control group; however, treatment with liposomal (SPB) hydroalcoholic extract significantly reduced AST and ALT's activity. Increases in MDA, TBIL, and NO levels and T-SH content due to BDL were restored to control levels by liposomal (SPB) hydroalcoholic extract treatment. Similarly, hepatic and plasma oxidative marker MDA levels, significantly enhanced by BDL, were significantly decreased by liposomal (SPB) hydroalcoholic extract treatment. Moreover, histopathological findings further demonstrated a significant decrease in hepatic damage in the liposomal (SPB) hydroalcoholic extract-treated BDL group. In addition, liposomal (SPB) hydroalcoholic extract treatment decreased the liver expression of inflammatory cytokines (IL-1β, TNF-α) and liver fibrosis markers (TGF-β and SM-α). Since liposomal (SPB) hydroalcoholic extract treatment alleviated the BDL-induced injury of the liver and improved the hepatic structure and function more efficiently in comparison to free SPB hydroalcoholic extract, probable liposomal (SPB) hydroalcoholic extract exhibits required potential therapeutic value in protecting the liver against BDL-caused oxidative injury.
Highlights
Nowadays, millions of people suffer from chronic or acute liver disorders [1]
Measured size for liposomal extract by dynamic light scattering (DLS) analysis was about 173 nm which is significantly greater than transmission electron microscopy (TEM) size, because of the fact that DLS analysis measures hydrodynamic size of nanoparticles
bile duct ligation (BDL) rats treated with liposomal-Stachys pilifera Benth (SPB) hydroalcoholic extract markedly reduced AST activity in comparison to the BDL group (P ≤ 0:05)
Summary
Hepatic cholestasis is a common pathophysiological disorder that leads to the toxic build-up of biliary salts in the liver [2]. The mechanism of fibrosis in liver cholestasis is not well understood [5]; various factors such as oxidative stress, transport disorders, immune suppression, and inflammatory injury can cause cholestasis [6]. The accumulation of biliary salts in the hepatic membrane increases the reactive oxygen species (ROS) content and subsequently causes oxidative stress leading to cell destruction [8, 9]. Pathophysiological conditions induced by bile duct ligation (BDL) resemble those exhibited by cholestasis, where it causes elevation of bile acid concentration and lipid peroxidation, as well as stimulation of inflammatory cells and phagocytic capacity of polymorphonuclear leukocytes [11]. Anticholestatic potentials of medicinal herbs have gained extensive attention [6, 9]
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