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Hepatic steatosis is the most common phenomenon of lipid metabolism disorder in farmed fish, but its molecular mechanism is poorly understood. Therefore, the present study was aimed to investigate steatosis induced by high-fat diet (HFD) and explore underlying mechanism in tilapia. The fish were fed on control diet or HFD for 90 days. The blood and liver tissues were collected to determine biochemical parameters, genes expression and proteins level after 30, 60 and 90 days and analyzed lipid accumulation, endoplasmic reticulum (ER) stress and autophagy. After 30 days of feeding, the plasma and hepatic lipid content (TG, TCH, LDL-C and HDL-C) and fatty acids (FAs) transportation (fabp1 and CD36) were enhanced significantly in HFD-fed tilapia. After 60 days, the lipid metabolism disorder, such as increase of TG synthesis and free CH formation, and decrease of FAs β-oxidation and biosynthesis, was observed in liver of HFD-fed tilapia. Further, with increasing lipid accumulation, ER stress was induced and worsen hepatic steatosis via activating IRE1 signaling pathway in liver of HFD group after 90 days. Meanwhile, the autophagy was suppressed via impairing AMPK and BFET pathways in HFD-fed tilapia liver after 90 days. Our results demonstrated that HFD feeding induced extensive lipid deposition, promoted ER stress, suppressed autophagy in tilapia liver. Interestingly, these pathological features were positively correlated with the duration of HFD feeding.

In order to investigate the mode of action of Yimu Shenghuasan preparation in endometrial cells of dairy cows, the primary cultured endometrial cells in cows were isolated and the inflammatory models were made by lipopolysaccharide (LPS) induction. The inflammatory cells were treated with gradient concentration of herbal medicine preparation, Yimu Shenghuasan for 48 and 72 h. The expression of cytochrome P450 (CYP450) was detected by Western blot. The amounts of IgG and IgA in sera were also detected in the endometritis of dairy cows. The expression level of CYP450 in the endometrial cells of dairy cow was increased gradually, and the amounts of IgG, IgA were increased significantly as compared with those in the control group. The expression level of CYP450 in the inflammatory cells was increased significantly in the treatment of 2 000 μg mL −1 of Yimu Shenghuasan after 48 h of treatment.

Grass carp hemorrhage is an acute contagious disease caused by grass carp reovirus (GCRV). The pathogenesis of GCRV and the relationship between GCRV and the host cells remain unclear. The aim of the present study was to investigate the relations among apoptosis, intracellular oxidative stress and virus replication in GCRV infected-cells. The results showed that GCRV induced activation of caspase proteases as early as 12 h, and reached maximum activities at 24 h or 48 h post-infection in a grass carp kidney cell line (CIK cells). Meanwhile, the levels of tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β) also were increased in GCRV-infected CIK cells and showed a statistically significant difference from 24 h to 96 h post-infection. The infection of GCRV caused the destruction of entire monolayer and the death of host cells. Accompanied by the infection, a severe oxidative stress occurred, which led to extensive loss of antioxidants and formation of lipid peroxidation after 48 h post-infection. These data suggested that the apoptosis which was triggered at an early stage (12-24 h) in the viral infection cycle, might be independent of virus replication, while the oxidative stress induced by GCRV was mostly related to the virus replication.

In the present study, the cellular and molecular mechanism of carbon tetrachloride (CCl4)-induced hepatotoxicity in fish was investigated by studying the effects of CCl4 on the oxidative stress, inflammatory response and hepatocyte apoptosis. Common carp were given an intraperitoneal injection of 30% CCl4 in arachis oil (0.5ml/kg body weight). At 72h post-injection, blood were collected to measure glutamate pyruvate transaminase (GPT), glutamate oxalate transaminase (GOT), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), total antioxidant capacity (T-AOC) and malondialdehyde (MDA), liver samples were taken to analyze toll-like receptor 4 (TLR4), cytochrome P450 2E1 (CYP2E1) and gene expressions of inflammatory cytokines and nuclear factor-κB (NF-κB/cREL). Cell viability and apoptosis were analyzed after treatment of the primary hepatocytes with CCl4 at 8mM. The results showed that CCl4 significantly increased the levels of GPT, GOT, MDA, TLR4 and CYP2E1, reduced the levels of SOD, GPx, CAT, GSH and T-AOC, and up-regulated the gene expressions of NF-κB/cREL and inflammatory cytokines including tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), IL-1β, IL-6 and IL-12. In vitro, CCl4 caused a dramatic loss in cell viability and induced hepatocyte apoptosis. Overall results suggest that oxidative stress lipid peroxidation, and TNF-α/NF-κB and TRL4/NF-κB signaling pathways play important roles in CCl4-induced hepatotoxicity in fish.