R. verniciflua and E. ulmoides Extract (ILF-RE) Protects against Chronic CCl4-Induced Liver Damage by Enhancing Antioxidation

Abstract

This study aimed to characterize the protective effects of R. verniciflua extract (ILF-R) and E. ulmoides extract (ILF-E), the combination called ILF-RE, against chronic CCl4-induced liver oxidative injury in rats, as well as to investigate the mechanism underlying hepatoprotection by ILF-RE against CCl4-induced hepatic dysfunction. Chronic hepatic stress was induced via intraperitoneal (IP) administration of a mixture of CCl4 (0.2 mL/100 g body weight) and olive oil [1:1(v/v)] twice a week for 4 weeks to rats. ILF-RE was administered orally at 40, 80, and 120 mg/kg to rats for 4 weeks. Alanine transaminase (ALT), aspartate transaminase (AST), gamma-glutamyl transpeptidase (GGT), and lipid peroxidation assays were performed, and total triglyceride, cholesterol, and LDL-cholesterol levels were quantified. Furthermore, ER stress and lipogenesis-related gene expression including sterol regulatory element-binding transcription factor 1 (SREBP-1), fatty acid synthase (FAS), and P-AMPK were assessed. ILF-RE markedly protected against liver damage by inhibiting oxidative stress and increasing antioxidant enzyme activity including glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase. Furthermore, hepatic dyslipidemia was regulated after ILF-RE administration. Moreover, hepatic lipid accumulation and its associated lipogenic genes, including those encoding SREBP-1 and FAS, were regulated after ILF-RE administration. This was accompanied by regulation of ER stress response signaling, suggesting a mechanism underlying ILF-RE-mediated hepatoprotection against lipid accumulation. The present results indicate that ILF-RE exerts hepatoprotective effects against chronic CCl4-induced dysfunction by suppressing hepatic oxidative stress and lipogenesis, suggesting that ILF-RE is a potential preventive/therapeutic natural product in treating hepatoxicity and associated dysfunction.

Protective Effect of Spore Powder of Antrodia camphorata ATCC 200183 on CCl4-Induced Liver Fibrosis in Mice

“…Recently, consumers have become more aware of the concept of consuming natural substances containing physiologically active compounds to prevent and treat diseases. Developing effective healthy foods for liver protection is of great significance for preventing and reducing the incidence rate of liver fibrosis, improving the life quality of patients and reducing mortality [4][5][6][7][8][9]. Antrodia camphorata, also known as niuzhangzhi, niuzhanggu, and zhangneigu in Chinese, is a unique and rare medicinal mushroom, which was initially found in the forests of Taiwan and has earned the names "Shenzhi" and "forest ruby" [10].…”

Hypotensive and Hepatoprotective Properties of the Polysaccharide-Stabilized Foaming Composition Containing Hydrolysate of Whey Proteins

“…Based on the determined in vitro and in vivo antioxidant activity of the WPH–PS composition it was proposed that its administration can alleviate effects of an oxidative stress to an organism. It is well known that a toxic dose of CCl 4 increases the concentration of reactive oxygen species (ROS) in the liver causing acute liver damage [ 46 , 47 , 48 ]. Hence, the in vivo antioxidant property of WPH–PS composition was assessed using a rat model with CCl 4 -induced hepatic injury ( Figure 5 ).…”

Citrus Peel Extract Ameliorates High-Fat Diet-Induced NAFLD via Activation of AMPK Signaling

“…On HFD, increased PERK/eIF2α branch is associated with the upregulation of SREBP-1 and its target protein FAS as well as with lipid accumulation ( Figure 5). The activation of AMPK, well-known physiological inhibitor of the energy-consuming mTOR signaling pathway [13][14][15], is a possible mechanism to explain the inhibition of mTOR/ER stress axis in NAFLD. Inactivation of AMPK activates the mTORC1 signaling pathway in HFD diet rats, leading to lipid accumulation.…”

“…The expressions of fatty acid synthase (FAS) and SREBP-1 were higher in the HFD group compared to NCD group, but CPEW (50 and 100 mg/kg) and CPEF (50 and 100 mg/kg) supplementation significantly reduced the expressions of these proteins ( Figure 5A). AMPK is suggested to be a therapeutic target for the treatment of obesity due to its role in the regulation of lipid metabolism [8,15]. Therefore, it is necessary to determine whether the activation of AMPK by CPEW and CPEF, prevents HFD-induced intracellular lipid accumulation by controlling the mTORC1-ER stress pathway.…”