To explore the mechanisms of diabetes mellitus (DM)-induced testicular injury caused by modulation of testicular glycolysis and gut microbiota (GM), and evaluation of the efficacy of catalpol in reversing testicular morbidity.
 
  A model of DM-induced testicular injury was established using a high-fat diet in KK-Ay mice. Microbial communities in the feces of mice in normal, model and catalpol (Cat) groups were analyzed by 16S gene sequencing. Correlations between the GM and lactate metabolism levels, lactate dehydrogenase activity, and indicators of testicular injury were analyzed.
 
  Cat significantly reduced general indicators of diabetes in mice with DM-induced reproductive injury, mitigated damage to the testicular tissue, and increased sperm count and motility. Additionally, the levels of products of glycolysis metabolism (e.g. lactate) increased following Cat treatment compared with the Model group. Disorders in the GM were also reversed in the Cat group.
 
  Cat ameliorated DM-induced testicular injury in KK-Ay mice by increasing the energy available to germ cells through glycolysis, principally through modulation of the GM and a reduction in the quantities of associated pathogenic bacteria.
 Cat ameliorated DM-induced testicular injury in KK-Ay mice by increasing the energy available to germ cells through glycolysis, principally through modulation of the GM and a reduction in the quantities of associated pathogenic bacteria.
  Lung cancer is a key contributor to the cancer-related death throughout the world. FGF21 (fibroblast growth factor 21) has been found to regulate various pulmonary diseases, whereas, the role and mechanism of FGF21 in lung cancer remain unclear. The aim of this research was to explore the expression and function of FGF21 in lung cancer.
 
  The mRNA and protein expression of FGF21 were analyzed through qRT-PCR and western blot, respectively. Cell proliferation, apoptosis and migration were analyzed by CCK-8 assay, flow cytometry and wound-healing assay, respectively. ROS, SOD, LDH and CK were examined with respective commercially kit.
 
  FGF21 level was increased in lung cancer tissue samples and cell lines at both mRNA and protein levels. Overexpressing FGF21 promoted cell growth and migration significantly. It also increased SOD and reduced ROS, LDH and CK contents. By contrast, down-regulated FGF21 presented the opposite effect on lung cancer cells. Furthermore, FGF21 may function as a tumor promotor by activating the SIRT1/PI3K/AKT signaling pathway in lung cancer.
 
  This study demonstrated that FGF21 was a tumor promoter in lung cancer development, serving as a feasible therapeutic target in the treatment of lung cancer.
 This study demonstrated that FGF21 was a tumor promoter in lung cancer development, serving as a feasible therapeutic target in the treatment of lung cancer.Prenatal exposure to arsenic is demonstrated to elevate the risk of brain damage and neurological disorders in the fetus, mainly due to its ability for crossing through the placental barriers.  https://www.selleckchem.com/  Increase in oxidative stress, inflammation, and DNA damage is main mechanisms of arsenic-induced neurotoxicity. Therefore, this study aimed to evaluate the neuroprotective effects of melatonin, as a potent anti-oxidant and anti-inflammatory agent against arsenic toxicity in the brains of male offspring rats. Pregnant mother rats were randomly assigned into four groups including group I, as control, group II received 10 mg/kg melatonin, group III received arsenic at 50 mg/kg, and group IV received melatonin and arsenic. After a two-month period, oxidative stress, DNA damage, inflammation and apoptosis were assessed in the male offspring rats. Exposure to arsenic significantly increased the pro-inflammatory and oxidative factors resulting in DNA damage and apoptosis in the brain tissues of offspring rats in comparison to controls (p less then 0.05). Exogenous administration of melatonin showed a significant increase in the tissue levels of acetylcholine esterase, decrease in the lactate dehydrogenase and myeloperoxidase, when compared to arsenic group (p less then 0.05). Melatonin also overcame the arsenic-induced oxidative stress and suppressed inflammation, DNA damage and apoptosis. Our results suggested that melatonin may be a promising neuro-protective agent and momentous therapy for the treatment of arsenic-toxicity in clinical conditions.Liver steatosis is one of the main drivers for the development of whole-body insulin resistance. Conversely, aerobic training (AT) has been suggested as non-pharmacological tool to improve liver steatosis, however, the underlying molecular mechanism remains unclear. Therefore, the aim of this study was to analyze the effect of 8-weeks AT in non-alcoholic liver disease (NAFLD) outcomes in obese mice. Male C57BL/6 J wild type (WT) were fed with standard (SD) or high-fat diet (HFD) for 12-weeks. Another group fed with HFD underwent 8-weeks of AT (60% of maximum velocity), initiated at the 5th week of experimental protocol. We measured metabolic, body composition parameters, protein and gene expression inflammatory and metabolic mediators. We found that AT attenuates the weight gain, but not body fat accumulation. AT improved triacylglycerol and non-esterified fatty acid plasma concentrations, and also whole-body insulin resistance. Regarding NAFLD, AT decreased the progression of macrovesicular steatosis and inflammation through the upregulation of AMPK Thr172 phosphorylation and PPAR-α protein expression. Moreover, although no effects of intervention in PPAR-γ protein concentration were observed, we found increased levels of its target genes Cd36 and Scd1 in exercised group, demonstrating augmented transcriptional activity. AT reduced liver cytokines concentrations, such as TNF-α, IL-10, MCP-1 and IL-6, regardless of increased Ser536 NF-κB phosphorylation. In fact, none of the interventions regulated NF-κB target genes Il1b and Cccl2, demonstrating its low transcriptional activity. Therefore, we conclude that AT attenuates the progression of liver macrovesicular steatosis and inflammation through AMPK-PPAR-α signaling and PPAR-γ activation, respectively, improving insulin resistance in obese mice.