Abstract
Both Lycium barbarum L. polysaccharides (LBP) and zinc have protective effects on liver injuries. In this paper, LBP and ZnSO4 were combined to study the effects on the prevention of alcoholic liver injury. The rats were divided into six groups, the normal group, alcohol group, zinc sulfate group, LBP group, low‐dose group of ZnSO4, and high‐dose group of ZnSO4 and LBP, used to explore the impact of LBP and ZnSO4 complex on liver lipid metabolism of alcohol, alcohol‐metabolizing enzymes, oxidative damage, and inflammation of the liver. The experimental model was established by gavage treatment, observation, and determination of indexes of rats. The results showed that the combination of LBP and ZnSO4 could significantly decrease the levels of triglyceride (TG), total cholesterol (TC), tumor necrosis factor‐α(TNF‐ɑ), malondialdehyde (MDA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and the activity of enzyme subtype 2E1 (CYP2E1). It also significantly increased the activities of total superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH‐Px), glutathione peptide (GSH), and alcohol dehydrogenase, effectively improved the liver tissue lesion. What is more, the combination of LBP and ZnSO4 had a synergistic effect on the remission of alcoholic fatty liver, and alleviated chronic alcoholic liver injury by promoting lipid metabolism, inhibiting oxidative stress, controlling inflammatory responses, and regulating the expression and activity of alcohol‐metabolizing enzymes in rats.
Highlights
Alcoholic liver disease (ALD) is due to excessive alcohol intake caused by liver damage and a series of lesions; the pathogenesis is more complex, making it become a worldwide medical problem (Corrao, Bagnardi, Zambon, & LaVecchia, 2004), which due to a high morbidity and mortality worldwide (Chiang & McCullough, 2014)
The results suggest that LBP group (D) and the complex of LBP and Zn group (E, F) can alleviate the symptom of weight loss in the model of alcoholic liver injury
The results showed that the combination of ZnSO4 and LBP had a synergistic effect on relieving lipid peroxide and chronic inflammation in rats
Summary
Alcoholic liver disease (ALD) is due to excessive alcohol intake caused by liver damage and a series of lesions; the pathogenesis is more complex, making it become a worldwide medical problem (Corrao, Bagnardi, Zambon, & LaVecchia, 2004), which due to a high morbidity and mortality worldwide (Chiang & McCullough, 2014). The main reason is that acetaldehyde, an intermediate alcohol metabolite, can deplete glutathione, accelerate lipid peroxidation, mitochondria damage, lead to oxidative stress (Ceni et al, 2014; Cheng & Kong, 2011). Alcohol‐derived reactive oxygen species (ROS) may directly trigger the systemic inflammatory response, activate nuclear factor kappa B (NF‐κB) simultaneously, which results in production of inflammatory cytokines, such as TNF‐α and IL‐6 (Cheng & Kong, 2011). Alcohol‐derived ROS may initiate a vicious cycle via the hepatocyte damage mechanism with additional inflammatory cytokines and ROS production (Ark, Lee, & Lee, 2014). No treatment has been approved for patients with ALD yet, and the only recognized management strategies were alcohol cessation (Orman et al, 2013); development of novel pathophysiological‐targeted adjuvant therapies are urgently needed (Ghorbani, Hajizadeh, & Hekmatdoost, 2016)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
