Effects of androgen deficiency on visceral fat accumulation and inflammatory gene expression in miniature pigs fed a high-fat diet / 中国实验动物学报

Objective The aim of this study was to explore the effect of androgen deficiency on serum hormone levels, visceral fat accumulation and inflammatory gene expression in miniature pigs fed a high-fat diet ( HFD) . Methods Sexually mature male Chinese Wuzhishan miniature pigs were divided into three groups ( animals/group) as follows:intact male pigs ( SHAM) , castrated male pigs ( CAS) and castrated male pigs plus testosterone treatment ( CAS+T) . The pigs were fed a HFD diet for 12 weeks. Serum levels of testosterone and leptin were measured and visceral fat were dissected and weighted. qRT?PCR was performed to determine the mRNA expression levels of lipogenic, lipolysis and inflammation relat?ed genes. Results (1) Serum testosterone levels were significantly decreased but serum leptin levels were significantly in?creased in the castrated pigs. These effects were recovered after testosterone treatment. ( 2 ) Visceral fat percentage was significantly increased in the castrated pigs, and testosterone treatment reduced the increased visceral fat in the castrated pigs. (3) Castration and testosterone treatment had no significant effects on the expression levels of lipogenic genes (FAS and ACC) and lipolysis genes (HSL and ATGL) in pigs fed a HFD. (5) Castration significantly induced the expressions of inflammatory genes including Leptin, CD68, CCL16, CCL23 and SAA, and testosterone treatment recovered the expres?sions of the above genes in the castrated pigs. Conclusions Castration?induced testosterone deficiency promotes visceral fat accumulation and upregulates the expression levels of inflammatory genes in miniature pigs fed a HFD. Moreover, tes?tosterone treatment ameliorates castration?induced visceral fat accumulation and inflammatory response in HFD?fed pigs.

TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation: pro-inflammatory response induced by their activation and their sensitization

Cutaneous neurogenic inflammation (CNI) is inflammation that is induced (or enhanced) in the skin by the release of neuropeptides from sensory nerve endings. Clinical manifestations are mainly sensory and vascular disorders such as pruritus and erythema. Transient receptor potential vanilloid 1 and ankyrin 1 (TRPV1 and TRPA1, respectively) are non-selective cation channels known to specifically participate in pain and CNI. Both TRPV1 and TRPA1 are co-expressed in a large subset of sensory nerves, where they integrate numerous noxious stimuli. It is now clear that the expression of both channels also extends far beyond the sensory nerves in the skin, occuring also in keratinocytes, mast cells, dendritic cells, and endothelial cells. In these non-neuronal cells, TRPV1 and TRPA1 also act as nociceptive sensors and potentiate the inflammatory process. This review discusses the role of TRPV1 and TRPA1 in the modulation of inflammatory genes that leads to or maintains CNI in sensory neurons and non-neuronal skin cells. In addition, this review provides a summary of current research on the intracellular sensitization pathways of both TRP channels by other endogenous inflammatory mediators that promote the self-maintenance of CNI.

Association between Interleukin-6 (-174 G/C and -572 C/G) Promoter Gene Polymorphisms and Risk of Intracerebral Hemorrhage in North Indian Population: A Case Control Study.

Background: Interleukin-6 (IL-6), a pro-inflammatory cytokine is involved in various vascular pathologies including stroke. Till date, no studies have been reported for the association between IL-6 gene polymorphisms with the risk of Intracerebral hemorrhage (ICH). Objective: The aim of this present case-control study was to investigate the association between IL-6 (-174 G/C and -572 C/G) gene polymorphisms and risk of ICH in North Indian population. Methods: Genotyping was carried out by using SNaPshot method for ICH patients and 100 age-sex matched ICH free controls. Conditional logistic regression analysis with adjusting multiple demographic and risk factor variables was used to calculate the strength of association between IL-6 (-174 G/C and -572 C/G) polymorphisms and risk of ICH. Results: Hypertension, diabetes, dyslipidemia, smoking and low socioeconomic status were found to be associated with the risk of ICH. The distribution of -174 G/C and -572 C/G genotypes was consistent with Hardy Weinberg Equilibrium (HWE) in the ICH and control subjects. Conditional logistic regression analysis showed a significant association between IL-6 -572 C/G gene polymorphism and the risk of ICH under dominant model (OR=3.7; 95%CI 1.05 to 13.1; p=0.004) and allelic model (OR=2.6; 95%CI 1.1 to 6.2; p=0.01). No significant association was observed for the association between IL-6 -174 G/C gene polymorphism and risk of ICH. Conclusion: Our results suggest that IL-6 (-572 C/G) polymorphism is significantly associated with the risk of ICH in North Indian population. Further prospective studies with large sample size are needed for independent validation.

The Expression of Inflammatory Gene in Exhausted Exercise Induced Myocardial Microinjury / 中国运动医学杂志

Objective To screening myocardial Inflammatory gene and its function in myocardial injury after single bout of exhausted exercises.Methods Fifry male Sprague-Dawley rats were randomly divided into sedentary control groups and single bout of exhausted exercise groups.Rats were killed at 0,6,12 and 24 h after single bout of exhausted exercises,and the gene chip technology was used to screening myocardial inflammatory gene.Results After single bout of exhausted exercise,myocardial inflammatory gene mainly involved with Cc117, PF4, CCL2, CCL21b, CCL7, Cc112_predicted, I16r, I11r2, Ifngr, Ccr12 predicted,ICAM-1 and Adamts1,with a trend of inrease to decrease.The gene expression of Ce117, PF4, Cc112_predicted, I116r, I11r2,Ifngr,Ccr12_predicted and Adamtsl shgnificant significant apgrade at oh after exercise,and the gene expression of CCL2,CCL21b,CCL7 and ICAM-1 showed significant upgrade at 6h after exercise.Conclusions The significantly increase expression of the chemotaetic factors and their receptors,mediate inflammdtory cells to the ischemia myocardium might be the patho-mechanism of exercise-induced yocardial micro damage after single bout of exhausted exercise.