These results suggest that neonatal CI stimulates the production of IL-1β and TNF-α through the TLR4/MyD88/NF-κB signalling pathway in the spinal cord, which contributed to visceral hypersensitivity induced by neonatal CI in rats.
The study was designed to examine the effects of calcitonin (CT) on the development of murine pre-implantation embryos and possible molecular mechanisms involved in the process. In the present study, the 2-cell embryos were treated with different concentration of CT in vitro for the indicated time and the results demonstrated that CT promoted the development of the pre-implantation embryos in a dosage-dependent manner by increasing the intracellular Ca(2+) level. Furthermore, the present study showed that CT significantly increased the expression of phospho-P38MAPK (Mitogen-Activated Protein Kinase) of the pre-implantation embryos by Western blots and pre-treatment of specific P38MAPK inhibitor significantly reduced the promotion effects of CT on the embryonic development in vitro culture. Moreover, the results of intrauterine horn injection showed that the average number of embryos implanted in CT-antibody or specific P38 MAPK inhibitor-treated uterus was significantly lower than that of the corresponding control, respectively. And the observation of tissue specimen suggested that some embryos were degenerated in CT-antibody or specific P38 MAPK inhibitor-treated uterus, and adipose vacuoles were present in the decidual cells. In conclusion, CT promoted the development of pre-implantation embryos and the intracellular Ca(2+) -dependent P38MAPK signal molecule was involved in the process.
ObjectiveTo investigate the influence and mechanism of combining exercise with diet control on a model of lipid metabolism rat induced by high fat diet.MethodsTwenty-four male Wistar rats were randomly divided into 3 groups of 8: normal, model and intervention. The model group and intervention group were fed with high fat diet, while the normal group received basal feed. From day 1, the intervention group was randomly given interventions such as swimming exercise and dietary restriction. The interventions duration were 28 days. At the end of the experiment, the levels of rats’ body weight and liver weight were detected, the serum levels of total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and hepatic triglyceride content (TG) were detected by using biochemical assay, serum level of gastrin (GAS), motilin (MTL) were assayed by the enzyme linked immunosorbent assay (ELISA).ResultsCompared with the level of body weight and liver weight in the normal rats, body weight and liver weight in the rat of the model group were significantly increase (P<0.05 or P<0.01). Plasma concentrations of TC, LDL-C and hepatic TG in the model group were significantly increased compared with those in the normal group (P<0.05 or P<0.01). The contents of GAS, MTL, HDL-C in the model rats’plasma were significantly reduced compared with those of the normal group (P<0.05 or P<0.01). Compared with those in the model group, rats’ body weight, liver weight, serum TC, LDL-C, and TG content of liver in the intervention group decreased significantly (P<0.05 or P<0.01). Meanwhile, serum content of GAS, MTL, HDL-C were significantly improved in the intervention rats compared to the model group.ConclusionThe action of combining exercise with diet control for lipid metabolism disorder might be related to regulation of GAS, MTL and other gastrointestinal hormones.
The present work provides evidence that HI insult destroyed brain cholesterol homeostasis, which might be important in the molecular pathology of hypoxic-ischemic white matter injury. Proinflammatory cytokines insulting oligodendrocytes, may cause cholesterol unbalance. Furthermore, specific therapeutic interventions to maintain brain cholesterol balance may be effective for the recovery of white matter function.
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