Objective To investigate the clinical significance of co-infection with hepatitis B virus ( HBV) and Epstein-Barr virus ( EBV) in HBV-related liver diseases such as chronic hepatitis B ( CHB) , liver cirrhosis, and hepatocellular carcinoma ( HCC) . Methods A retrospective analysis was performed for the clinical data of 487 patients with HBV infection who were diagnosed in Zhongnan Hospital of Wuhan University from May 2016 to August 2018, among whom 194 ( 39. 8%) had co-infection with HBV and EBV. The patients were divided into groups according to the copy number of EBV DNA ( > 400 IU/ml) , Child-Pugh class ( Child-Pugh class A, B, and C) , and progression of liver disease ( CHB, liver cirrhosis, and HCC) , and related indices were compared between groups. The t-test was used for comparison of normally distributed continuous data between two groups; an analysis of variance was used for comparison between multiple groups, and the least significant difference t-test was used for further comparison between two groups. The Kruskal-Wallis H test was used for comparison of non-normally distributed continuous data between groups, and the Dunn-Bonferroni test was used for further comparison between two groups. The chi-square test was used for comparison of categorical data between groups. Results The patients with CHB had a significantly higher copy number of HBV-DNA than those with liver cirrhosis or HCC ( t = 2. 417 and 3. 258, P = 0. 017 and 0. 001) , while the patients with HCC tended to have a higher copy number of EBV DNA than those with CHB or liver cirrhosis, but there was no significant difference between the three groups ( F = 1. 161, P = 0. 315) . After adjustment for liver function based on Child-Pugh class, the HCC patients with Child-Pugh class A liver function had a significantly higher copy number of EBV DNA than the CHB patients and the patients with liver cirrhosis ( t = 2. 062 and 2. 615, P = 0. 041 and 0. 010) , the liver cirrhosis patients with Child-Pugh class C liver function had a significantly higher copy number of EBV DNA than the CHB patients ( t = 2. 647, P = 0. 012) . ALT/AST, globulin, and lymphocyte percentage were specific clinical indices for co-infection with HBV and EBV. Conclusion There is an increase in EBV load in HCC patients, and both EBV and HBV are involved in the progression of liver diseases. Dynamic quantification of EBV DNA in patients with HBV infection has a certain significance in early intervention of the progression of liver diseases.

ObjectiveTo investigate the interventional effect of mangiferin on carbon tetrachloride (CCl4)-induced hepatic fibrosis in mice and the potential mechanism. MethodsA total of 45 male C57BL/6 mice were randomly divided into three groups: normal control group (NC group), liver fibrosis model group (CCl4 group), and mangiferin pretreatment group (CCl4+M group), with 15 mice in each group. An automatic biochemical analyzer was used to measure the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST); HE staining and Masson staining were performed to observe liver pathological changes; ELISA was used to measure the serum levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNFα); Western Blot was used to measure the protein expression of α-smooth muscle actin (α-SMA), nuclear factor-kappa B (NF-κB), IL-1β, p62, and microtubule-associated protein 1 light chain 3 (LC3) in the liver; quantitative real-time PCR was used to measure the mRNA expression of type I collagen (Col-I) and α-SMA in the liver. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups. ResultsHE staining and Masson staining showed a low proportion of mice with hepatocyte degeneration and necrosis and a significant reduction in collagen fibers in the CCl4+M group. Compared with the CCl4 group, the CCl4+M group had significant reductions in the serum levels of ALT and AST (both P＜001). ELISA showed that compared with the CCl4 group, the CCl4+M group had significant reductions in the serum levels of IL-1β, IL-6, and TNF-α (all P＜0.01). Western Blot showed that compared with the CCl4 group, the CCl4+M group had significant reductions in the protein expression of α-SMA, NF-κB, IL-1β, and LC3-II/I in the liver (P＜0.01, P＜0.05, P＜0.01, and P＜0.05) and a significant increase in the protein expression of p62 (P＜0.05). Quantitative real-time PCR showed that compared with the CCl4 group, the CCl4+M group had significant reductions in the mRNA expression of Col-I and α-SMA (P＜0.05 and P＜0.01). ConclusionMangiferin can alleviate CCl4-induced hepatic fibrosis in mice, possibly by reducing inflammation to protect liver function and inhibiting autophagy to reduce the activation of hepatic stellate cells.

Objective To investigate whether glucocorticoids, anti-tumor necrosis factor ( anti-TNF) drugs, and a past history of surgical treatment of inflammatory bowel disease ( IBD) are the risk factors for the coexistence of IBD and nonalcoholic fatty liver disease ( NAFLD) . Methods PubMed, Embase, Cochrane Library, Wanfang Data, CNKI, and VIP were searched for clinical trials of the coexistence of IBD and NAFLD published up to October 2018. The articles included were summarized and quality assessment was performed according to inclusion and exclusion criteria. RevMan 5. 2 was used for data processing; the random effects model was used for data with heterogeneity, and the fixed effect model was used for data with homogeneity. Results A total of 7 articles were included, with 1645 patients.The meta-analysis showed that glucocorticoids might not be a risk factor for the coexistence of IBD and NAFLD ( odds ratio ( OR) = 1. 19, 95% confidence interval ( CI) : 0. 90-1. 57, P = 0. 23) ; anti-TNF drugs were not a risk factor for the coexistence of IBD and NAFLD ( OR = 0. 86, 95% CI: 0. 65-1. 13, P = 0. 27) ; a past history of surgical treatment of IBD was a risk factor for the coexistence of IBD and NAFLD ( OR = 1. 50, 95% CI: 1. 09-2. 05, P = 0. 01) . Conclusion Glucocorticoids and anti-TNF drugs for the treatment of IBD may not increase the incidence rate of the coexistence of IBD and NAFLD, while surgical treatment for IBD may increase this incidence rate.

Objective To investigate the influence of low-lead high-fat diet on liver function and blood lipids in rats with nonalcoholic fatty liver disease ( NAFLD) , as well as the expression of sterol regulatory element-binding protein-1 c ( SREBP-1 c) , fatty acid synthase ( FAS) , and acetyl-CoA carboxylase α ( ACCα) in the liver from the aspect of the fatty acid synthesis pathway. Methods A total of 40 clean male Sprague-Dawley rats were given adaptive feeding for 14 days and were then randomly divided into normal group, low-lead exposure group, high-fat diet group, and low-lead high-fat diet group, with 10 rats in each group. The rats were sacrificed after 8 weeks of feeding with the corresponding diet, and serum and liver samples were collected to measure blood lead, liver function, blood lipids, and liver pathology. Western blot and RT-PCR were used to measure the protein and mRNA expression of SREBP-1 c, FAS, and ACCα involved in fatty acid synthesis. A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups. Results There were marked liver pathological changes after exposure. The sections from the normal group and the low-lead exposure group had a smooth surface and evenly distributed nuclei, without marked adipocyte infiltration or inflammatory response; the sections from the low-lead high-fat diet group and the high-fat diet group had marked fatty infiltration and inflammatory cell infiltration, and those from the low-lead high-fat diet group had larger fat vacuoles. There were significant differences in blood lead and liver lead between groups ( F = 37. 792 and 21. 458, both P < 0. 001) , and the low-lead exposure group and the low-lead high-fat diet group had significantly higher levels than the normal group ( all P < 0. 05) . There were significant differences in aspartate aminotransferase ( AST) , alanine aminotransferase ( ALT) , high-density lipoprotein cholesterol ( HDL-C) , and low-density lipoprotein cholesterol ( LDL-C) between groups ( F = 35. 791, 24. 422, 37. 287, and 42. 371, all P <0. 001) , and the low-lead exposure group, the high-fat diet group, and the low-lead high-fat diet group had significantly higher AST, ALT, LDL-C, and HDL-C than the normal group ( all P < 0. 05) . Western blot and RT-PCR showed consistent protein and mRNA expression features of SREBP-1 c, FAS, and ACCα, and there were significant differences in the protein and mRNA expression of REBP-1 c, FAS, and ACCα between groups ( protein expression: F = 21. 864, 22. 358, and 57. 761, all P < 0. 001; mRNA expression: F =34. 652, 22. 964, and 42. 384, all P < 0. 001) . Compared with the normal group and the low-lead exposure group, the high-fat diet group and the low-lead high-fat diet group had significant increases in the protein and mRNA expression of SREBP-1 c, FAS, and ACCαin the liver ( all P < 0. 05) . Conclusion Low-lead exposure can aggravate liver function and dyslipidemia in NAFLD rats, possibly by regulating the expression of SREBP-1 c, FAS, and ACCα.

Objective To investigate the protective mechanism of mild hypothermia pretreatment against hepatic ischemia-reperfusion injury in rats. Methods A total of 40 male Sprague-Dawley rats were randomly divided into sham-operation group ( Sham group) , hepatic ischemia-reperfusion injury group ( HIRI group) , mild hypothermia group ( MH group) , and mild hypothermia + LY294002 group ( MH +LY group) , with 10 rats in each group. Serum and liver tissue samples were collected at 3, 6, 12, and 24 hours of hepatic ischemia-reperfusion. Western blotting was used to measure the protein expression of phosphoinositide 3-kinase ( PI3 K) , phosphorylated PI3 K ( p-PI3 K) , protein kinase-B ( Akt) , and phosphorylated Akt ( p-Akt, Ser308) in liver tissue. TUNEL and Western blotting were used to measure cell apoptosis and expression of apoptosis-related proteins in liver tissue. ELISA was used to measure the levels of superoxide dismutase ( SOD) , glutathione peroxidase ( GSH-Px) , and malondialdehyde ( MDA) in liver tissue. An automatic biochemical analyzer was used to measure the activities of alanine aminotransferase ( ALT) and aspartate aminotransferase ( AST) in serum. A one-way analysis of variance was used for comparison between multiple groups, and the SNK-q test was used for further comparison between two groups.Results The HIRI group had significantly lower relative expression levels of p-PI3 K and p-Akt than the Sham group ( q = 5. 217 and5. 456, both P < 0. 01) , and the MH group had significantly higher relative expression levels of p-PI3 K and p-Akt in liver tissue than the HIRI group ( q = 10. 434 and 14. 116, both P < 0. 01) . At 3, 6, 12, and 24 hours of hepatic ischemia-reperfusion, the HIRI group, the MH group, and the MH + LY group had significantly higher activities of AST and ALT in serum than the Sham group ( all P < 0. 001) .TUNEL staining showed that the HIRI group had a significantly higher proportion of apoptotic cells in liver tissue than the Sham group ( 42. 25% ± 3. 50% vs 3. 21% ± 0. 5%, q = 10. 187, P < 0. 01) . Compared with the HIRI group, the MH group had a significant reduction in the proportion of apoptotic cells ( q = 7. 784, P < 0. 01) , while there was no significant difference in the proportion of apoptotic cells between the HIRI group and the MH + LY group ( 42. 25% ± 3. 50% vs 38. 19% ± 2. 8%, q = 1. 059, P > 0. 05) . Western blotting showed that compared with the Sham group, the HIRI group had a significant reduction in the expression of the anti-apoptotic protein Bcl-2 ( q =2. 101, P < 0. 05) and significant increases in the expression of the pro-apoptotic proteins Bax, Fas, and Fasl ( q = 11. 016、4. 735, and10. 201, all P < 0. 01) , and the regulatory effect of HIRI on apoptotic-related proteins was downregulated by mild hypothermia treatment.According to the results of oxidative indices, the HIRI group, the MH group, and the MH + LY group had significantly lower expression of SOD and GSH-Px and significantly higher expression of MDA in liver tissue than the Sham group ( all P < 0. 05) ; compared with the HIRI group, the MH group had significantly higher expression of SOD and GSH-Px ( q = 2. 894 and 2. 731, both P < 0. 05) and significantly lower expression of MDA ( q = 5. 888, P < 0. 05) in liver tissue. In addition, mild hypothermia + LY294002 treatment significantly reduced the regulatory effect on the expression of SOD, MDA, and GSH-Px in liver tissue in the MH group ( q = 2. 999, 2. 944, and 2. 620, all P < 0. 05) . Conclusion MH exerts a protective effect against HIRI in rats, possibly by activating the PI3 K/Akt pathway to downregulate hepatocyte apoptosis and enhance antioxidant capacity in vivo.