Impact of JNK inhibitor XG-102 in a diet-induced rat model of non-alcoholic steatohepatitis / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To observe the impact of the JNK inhibitor XG-102 in a diet-induced rat model of non-alcoholic steatohepatitis.</p><p><b>METHODS</b>Forty-eight Sprague-Dawley male rats were subjected to a percutaneous superior mesenteric vein retention catheter operation and fed with a standard diet for 10 days, after which the rats were randomly divided into the following three groups: normal control (NC) group; high-fat (HF) model group; XG-102 treatment group. The HF group was fed an HF diet and treated with 0.9% sodium chloride for 16 weeks. The XG-102 group was fed an HF diet for 16 weeks and simultaneously treated with XG-102 (1 mg/kg) once per day for 4 weeks. The levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglyceride (TG), homeostasis model of assessment insulin resistance (HOMA-IR) and tumor necrosis factor-alpha (TNFa) were measured. Liver histological changes were observed. The protein expressions of phospho-c-Jun and cleaved caspase-3 were detected by western blotting.</p><p><b>RESULTS</b>Compared with the NC group, the HF group showed significantly higher levels of serum ALT, AST, TC, TG, HOMA-IR and TNFa (P<0.05). Compared with the HF group, the XG-102 group showed significantly lower levels of serum ALT, AST, TC, TG, HOMA-IR and TNFa (P<0.05). The HF group also showed significantly higher protein expression of phospho-c-Jun and cleaved caspase-3 than the NC group (P<0.05) and the XG-102 group (P<0.05).</p><p><b>CONCLUSION</b>The JNK inhibitor XG-102 may ameliorate lipid metabolism, reduce insulin resistance, decrease liver injury and inhibit hepatocytes apoptosis.</p>

THE PATHOLOGY OF DOGS′ FACIAL NERVE AFTER SIMULATED EXPLOSIVE WOUND OF MAXILLOFACIAL REGION / 解放军医学杂志

To observe the injury process and pathological changes of the facial nerve,a primer was detonated at a distance of 10 cm from the face of each of 36 anesthelized dogs to simulate blast injury of the maxillofacial region. At the same time, a tangential wound of masseter was produced by a steel pellet fired with a musket to simulate a shrapnel injury. At different time points after injury, the action potential of the facial nerves was checke d and the pathological changes in axons and neurons of facial nerves were observed after HE and Nissle′s staining,respectively.One day after the injury,the facial nerve axons were found to be disrupted extensively,although the epineurium was still in continuity. There were degeneration and necrosis of neurons with infiltration of inflammatory cells in the facial nerve.One week later, the inflammation began to become milder, and the necrotic neurons were gradually absorbed. Four weeks later, the survived neurons appeared normal, and axons began to regenerate. Meanwhile, electromyography (EMG) showed that the action potential of facial nerve recovered. All the observations suggested that severe indirect injury to the facial nerve trunks in an explosive injury was the main pathological changes which involved an extensive area with severe damage in neurons.