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  • In addition the TAA treated groups show

    2019-06-24

    In addition, the TAA-treated groups showed a significant reduction in body weight with significantly increased liver weights and sizes compared to control rats, but NJ cotreatment reversed those defects (Table 1). The reduction in body weights could be attributed to the toxic effect of TAA throughout the period of the experiment. Moreover, TAA altered fatty Cilostazol composition in tissues, thus decreasing fatty acid biosynthesis in the liver and lowering serum TAG levels. It has been reported that an improvement in serum lipids and oxidative status in high-cholesterol/fat dietary hamsters treated with NJ is highly related to the regulation of lipid homeostasis by the phytochemicals in NJ. Pallottini et al also indicated that TAA reduces the 3-hydroxy-3-methylgltaryl coenzyme A reductase activity, which may explain the lower serum TC level observed in rats treated with TAA (Fig. 1). Furthermore, the TAA group strongly showed a significant elevation of liver TC and TAG levels in comparison to NJ-cotreated groups (Fig. 2). Fatty acid accumulation also leads to the induction of ER stress and ROS formation, which again hastens the hepatic injury. TAA-induced liver fibrosis is caused by free radical-mediated lipid peroxidation. Lipid peroxidation occurs during the processes of liver fibrosis and inflammation. ROS generation, mitochondrial dysfunction, and antioxidant insufficiency have been reported to advance the development of liver cirrhosis. Thus, oxidative stress also triggers production of inflammatory cytokines, causes inflammatory and fibrogenic responses, and is recognized as being of major importance in the progression of this disease. The current study demonstrated that TAA-treated rats exhibit an increase in hepatic TBARS values and a decrease in the reduced GSH content as compared to control rats, suggesting the impairment of hepatic antioxidant capabilities. Our results showed that NJ supplementation can decrease the liver TBARS values but increase the content of reduced GSH in the liver, as well as SOD, CAT, and GSH-Px activities in TAA-treated rats (Table 2). Those benefits should result from the bioactive compounds, i.e., polyphenols, polysaccharides, Se, Mn, etc., in NJ. Also, NJ cotreatment effectively reduced serum ALT and AST levels (Fig. 1), hepatic fibrosis scores (Fig. 3B), the gene expressions of iNOS, Bip, IRE1, XBP-1, and ATF4 in livers (Fig. 4A), and hepatic IL-1β contents (Table 2) and collagen accumulation (Fig. 2B) in TAA-treated rats. Therefore, an antiinflammatory or antifibrosis effect of NJ against a TAA induction could correspond highly to the reduction of liver oxidative levels. Oxidative stress triggers ER stress and unfolded protein response, however, excessive or prolonged ER stress decreases the mitochondrial membrane potential, limits bioenergetics changes, and fosters the generation of ROS, ultimately inducing apoptosis. Naturally fermented NJ contains plenty of polysaccharides, polyphenols, and some trace minerals (Zn, Mn, and Se). Natural polysaccharides, largely found in fruits and vegetables, have been confirmed to play a vital role as free radical scavengers. It has also been demonstrated that polysaccharides and polyphenols are synergistic in the reduction of serum leptin levels and antiinflammatory activities. Trace minerals Mn and Se are cofactors for SOD and GSH-Px, respectively. Zn has antioxidant and anticancer activities and helps to reduce cardiovascular disease. Moreover, activated HSCs can downregulate tissue TIMPs, leading to a hypothesis that matrix degradation is inhibited during progressive fibrosis. Our results showed that TAA induces proinflammatory responses, as evidenced by increased ROS production, cytokine release (TNF-α and IL-1β; Table 2), and matrix degrading enzyme activation (MMP-9 and MMP-2; Fig. 4C).The TIMP-1 inhibition may not be maximal and MMP-mediated degradation still occurs in remodeling during progressive fibrosis. Hence, NJ cotreatment exerts hepatoprotective effects against TAA damage, possibly via downregulation of MMP-2 and MMP-9 activities and upregulation of TIMP-1 and TIMP-3 (Figs. 4B and 4C). Taken together, these data strongly suggest that the ameliorative effect of NJ on liver fibrotic tissues is potentially due to a regulation of MMP-9-mediated degradation, where an active MMP-9 could be inhibited by an interaction with TIMP-1and TIMP-3 in vivo.