The present study assessed the possible mechanisms by which the insulin regulates the heat shock (HSPs) and transitional proteins expression and consequently ameliorates the oxidative stress-induced damages in germ and sperm cells DNA contents. Mature male Wistar rats were distributed into control, Hyperglycemia-induced (HG) and insulin-treated HG-induced (HG-I) groups. Following 8weeks from HG induction, testicular total antioxidant capacity (TAC), immunoreactivity of 8-oxodG, germ cells mRNA damage, Hsp70-2a, Hsp90, transitional proteins 1 and 2 (TP-1 and -2) mRNA and protein expressions were analyzed. Moreover, the sperm chromatin condensation was assessed by aniline-blue staining, and DNA integrity of germ and sperm cells were analyzed by TUNEL and acrdine-orange staining techniques. The HG animals exhibited significant (p<0.05) reduction in TAC, HSp70-2a, TP-1 and TP-2 expression levels, and increment in 8-oxodG immunoreactivity, mRNA damage, and Hsp90 expression. However, insulin treatment resulted in (p<0.05) enhanced TAC level, Hsp70-2a, Hsp90, TP-1 and TP-2 expressions, besides reduced 8-oxodG immunoreactivity and mRNA damage compared to the HG group (p<0.05). The chromatin condensation and the germ and sperm cells DNA fragmentation were decreased in HG-I group. Insulin treatment amplifies the testicular TAC level, improves the Hsp70-2a, TP-1, and TP-2 expressions, and boosts the Hsp90-mediated role in DNA repairment process. Consequently, altogether could maintain the HG-induced DNA integrity in the testicular and sperm cells.Insulin treatment amplifies the testicular TAC level, improves the Hsp70-2a, TP-1, and TP-2 expressions, and boosts the Hsp90-mediated role in DNA repairment process. Consequently, altogether could maintain the HG-induced DNA integrity in the testicular and sperm cells.In clinical and laboratory practice, the use of anesthetics is essential in order to perform surgeries. Anesthetics, besides causing sedation and muscle relaxation, promote several physiological outcomes, such as psychotomimetic alterations, increased heart rate, and blood pressure. However, studies depicting the behavioral effect induced by ketamine and isoflurane are conflicting. OSMI-4 purchase In the present study, we assessed the behavioral effects precipitated by ketamine and isoflurane administration. We have also evaluated the ketamine effect on cell cytotoxicity and viability in an amygdalar neuronal primary cell culture. Ketamine (80 mg/kg) caused an anxiogenic effect in rats exposed to the elevated T-maze test (ETM) 2 and 7 days after ketamine administration. Ketamine (40 and 80 mg/kg) administration also decreased panic-like behavior in the ETM. In the light/dark test, ketamine had an anxiogenic effect. Isoflurane did not change animal behavior on the ETM. Neither ketamine nor isoflurane changed the spontaneous locomotor activity in the open field test. However, isoflurane-treated animals explored less frequently the OF central area seven days after treatment. Neither anesthetic caused oxidative damage in the liver. Ketamine also reduced cellular metabolism and led to neuronal death in amygdalar primary cell cultures. Thus, our work provides evidence that ketamine and isoflurane induce pronounced long lasting anxiety-related behaviors in male rats. Immunosuppressive myeloid-derived suppressor cells (MDSCs) continuously expand and lead to poor outcome during sepsis. The activation of liver X receptor (LXR) can mitigate sepsis-induced liver and myocardial damage. This study aims to determine whether LXR plays a protective role in sepsis by regulating MDSCs. Cecal ligation and puncture(CLP)was used to induce sepsis in mice. The mice were then treated with LXR agonist GW3965 (3mg/kg) or vehicle 1h, 6h, 12h, 24h, 48h, 72h postoperatively. The effect of LXR on the survival rate and multi-organ injury induced by sepsis was evaluated by survival analysis, histological staining, biochemical analysis and ELISAs. The percentages of MDSCs and T cells were detected using flow cytometry. The mRNA expressions of LXR and ATP-binding cassette transporter A1 (ABCA1) were measured using real-time quantitative PCR (RT-qPCR). ABCA1 protein level was determined using immunofluorescence staining. LXR agonist GW3965 treatment improved the survival of septic mice, accompanied by reduced multi-organ injury and a decreased level of inflammatory cytokines. Furthermore, GW3965 treatment decreased MDSCs abundance in spleen by boosting the apoptosis of spleen MDSCs, therefore ameliorating their immunosuppressive activity. Meanwhile, bacteria clearance in tissues was enhanced after the GW3965 administration in septic mice. Mechanistically, GW3965 activated LXRβ and its downstream target ABCA1 to initiate the apoptosis of spleen MDSCs. These findings provide new insights into the relationship between LXR and MDSCs in sepsis, thus revealing a potentially effective approach to target the immunosuppression of sepsis.These findings provide new insights into the relationship between LXR and MDSCs in sepsis, thus revealing a potentially effective approach to target the immunosuppression of sepsis.Over the past few years, tumor immunotherapy has emerged as an innovative tumor treatment and owned incomparable advantages over other tumor therapy. With unique complexity and uncertainty, immunotherapy still need helper to apply in the clinic. Galectins, modulated in tumor microenvironment, can regulate the disorders of innate and adaptive immune system resisting tumor growth. Considering the role of galectins in tumor immunosuppression, combination therapy of targeted anti-galectins and immunotherapy may be a promising tumor treatment. This brief review summarizes the expression and immune functions of different galectins in tumor microenvironment and discusses the potential value of anti-galectins in combination with checkpoint inhibitors in tumor immunotherapy.As an ambiguous member of vascular endothelial growth factor family, VEGF-B has long been poorly understood in its function. Recent researches showed VEGF-B isoforms exerted their metabolic effect through indirectly activating the VEGF-A/VEGFR2 pathway. Here, we report the lipid-lowing effect of VEGF-B via VEGFR1. We investigated the effect of VEGF-B on lipid metabolism in vivo and in vitro approaches. Treatment of mice with VEGF-B recombinant protein repressed HFD-induced body weight gain. This treatment also alleviated obesity associated hyperlipidemia and fatty liver disease. In the muscle and liver of VEGF-B-treated HFD mice were observed increased protein expression of carnitine palmitoyltransferase-1 (CPT-1) and the phosphorylation of ACC and AMP-activated protein kinase (AMPK). This effect was confirmed in HepG2 cells incubated with VEFG-B in which the increased AMPK activation and CPT-1 expression occurs due to activation of Calcium/calmodulin-dependent Protein Kinase β (CaMKKβ) by VEFG-B. VEGF-B increased expression of key genes responsible for lipid oxidation while reducing those for fatty acid synthesis in vivo and in vitro.