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Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases and also the main cause of liver cirrhosis and hepatocellular carcinoma. Cav3.2 channel is an important member of T-type calcium channel and plays a vital role in energy and metabolic balance. However, the effects of Cav3.2 on NFALD remain unclear. Here, we aimed to investigate the function of Cav3.2 channel in the development and progression of NAFLD. After 16 weeks on a high-fat diets (HFD), Cav3.2 knockout (Cav3.2 KO) improves hepatic steatosis, liver injury and metabolic syndrome in NAFLD mice model. We provided evidence that Cav3.2 KO inhibited HFD-induced hepatic oxidative damage, inflammation and hepatocyte apoptosis. In addition, Cav3.2 KO also attenuated the hepatic lipid accumulation, oxidative damage, inflammation and hepatocyte apoptosis in palmitic acid/oleic acid (PAOA)-treated primary hepatocytes. Further, Cav3.2 KO-mediated liver protection function were dependent on its interaction with CaMKII signaling. These results suggest that therapeutic approaches targeting Cav3.2 provide effective approaches for treating NAFLD.

A recent study showed that peroxiredoxins (Prxs) play an important role in the development of pathological cardiac hypertrophy. However, the involvement of Prx5 in cardiac hypertrophy remains unclear. Therefore, this study is aimed at investigating the role and mechanisms of Prx5 in pathological cardiac hypertrophy and dysfunction. Transverse aortic constriction (TAC) surgery was performed to establish a pressure overload-induced cardiac hypertrophy model. In this study, we found that Prx5 expression was upregulated in hypertrophic hearts and cardiomyocytes. In addition, Prx5 knockdown accelerated pressure overload-induced cardiac hypertrophy and dysfunction in mice by activating oxidative stress and cardiomyocyte apoptosis. Importantly, heart deterioration caused by Prx5 knockdown was related to mitogen-activated protein kinase (MAPK) pathway activation. These findings suggest that Prx5 could be a novel target for treating cardiac hypertrophy and heart failure.

Background. Comparing the effect of two different κ-receptor agonists, nalbuphine and oxycodone, and regular morphine in patients for prophylactic analgesia of acute pain after daytime laparoscopic cholecystectomy. Methods. One hundred and twenty-four patients undergoing laparoscopic cholecystectomy were randomly allocated to receive nalbuphine (group N), oxycodone (group O), and morphine (group M). The three groups were all given intravenous injection (iv.) of 0.15 mg/kg injection before incision and 0.05 mg/kg injection at the end of pneumoperitoneum. The Visual Analogue Scale (VAS) scores (incision, visceral, and shoulder) and Ramsay sedation scores at 1, 2, 4, 8, 12, 16, 20, and 24 hours after surgery, the time of extubation, the incidence of postoperative adverse events, the satisfaction of pain treatment, and the duration of stay after surgery were all recorded. Results. Compared with group M, the VAS scores of visceral pain at rest decreased in group N and group O at 1-8 h after surgery ( P < 0.05 ). The VAS scores of visceral pain at movement in group N decreased longer than those in group O ( P < 0.05 ). Compared with that of group M, the postoperative time in Ramsay sedation score of group O increased longer than that of group N ( P < 0.05 ). Compared with group N, patients had worse sleep quality in group O, longer length of stay in group M, and lower satisfaction in both groups. Conclusion. Compared with morphine, prophylactic use of the κ-receptor agonists, nalbuphine and oxycodone, during laparoscopic cholecystectomy can reduce postoperative visceral pain. Furthermore, the nalbuphine group had fewer adverse reactions, better analgesia, and better satisfaction.