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Abstract@#School based lifestyle interventions have many advantages, which can effectively reduce the prevalence of overweight and obesity, improve children and their families knowledge of overweight and obesity, and enhance their cognition of behaviors related to energy balance. Moreover, it can improve the level of cardiometabolic risk (CMR). By searching PubMed, CNKI and Wanfang databases, the article review the effects of school based physical activity and dietary interventions on children s blood pressure, blood lipids, blood glucose, and other CMR indicators, and analyze the differences among different groups of people, such as gender, age, and race, in order to provide the evidence for future school based intervention studies on overweight and obesity in children.
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Aim To investigate the role of eNOS/PKG- 1 pathway in L-arginine (L-arg) intervention in right ventricular remodeling induced by monocrotaline (MCT) in Sprague Dawley (SD) rats with the aid of the tool medicine L-NAME. Methods Twenty SD rats were randomly divided into control group, MCT group, L-Arg group and L-Arg + L-NAME group. The general condition of rats was observed; the right ventricular pressure of rats was measured by right heart catheterization; the rats and the right ventricle were weighed and the right ventricular mass index was calculated; the morphological changes of the right ventricular were observed by H&E staining; the protein expressions of cTnl, eNOS and PKG-1 were detected by Western blot in the right ventricular. Results Compared with control group, right ventricular max pressure and right ventricular mass index significantly increased ( P < 05) ; the weight of rats in MCT group was significantly reduced ( P < 0. 05); the right ventricular myocytes were hypertrophic, disordered and infiltrated with inflammatory cells; the protein expression of cTnl was obviously up-regulated ( P < 0. 05 ) ; the protein expressions of eNOS and PKG-1 were significantly down- regulated ( P < 0. 05 ) . L-arg could significantly improve the above changes ( P < 0. 05 ). However, the effects of L-arg were inhibited by eNOS inhibitor L- NAME. Conclusions L-arg can improve the right ventricular remodeling in rats induced by MCT, and the mechanism may be related to the up-regulation of the protein levels of eNOS and PKG-1.
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Abstract; Aim To explore the effect of icariin (ISO) in mice. Methods C57BL/6 mice were ran- (ICA) on myocardial fibrosis induced by isoproterenol domly divided into control group, ISO group, low-dose (15 mg • kg"1), middle-dose (30 mg • kg"1) and high-dose (60 mg • kg"1) of ICA-treated group and Losartan-treated group ( 9 mg • kg"1 ). The control group was subcutaneously injected with normal saline, and the other groups were subcutaneously injected with ISO (5 mg • kg"1, qd) continuously 14 days to established the myocardial fibrosis model. The ICA-treated groups and Losartan-treated group were simultaneously intragastrically administered of ICA or Losartan, respectively. And the other groups received the same a- mount of double distilled water. The left ventricular e- jection fraction (LVEF) and the left ventricular fraction shortening rate ( LVFS) were evaluated by the small animal ultrasound. The heart mass index (HMI) was calculated. The left ventricular collagen deposition was detected by Masson staining. The protein expressions of a-SMA, MMP-2, MMP-9 and TIMP-1 in the left ventricular tissue were detected by Western blot. Results ICA (30, 60 mg • kg"1) and Losartan could inhibit the decreased LVEF and LVFS, the increased HMI and left ventricular collagen deposition, the up- regulated a-SMA and MMP-9 protein expression, the down-regulated MMP-2 and TIMP-1 protein expression in the left ventricular tissues induced by ISO. Conclusions ICA can improve myocardial fibrosis induced by ISO in mice, and the underlying mechanism may be related to the regulation of the protein expression of a- SMA and MMPs/TIMP-1.
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Aim To investigate the effects of IcarisideⅡ ( ICS Ⅱ) on myocardial fibrosis in spontaneously hypertensive rat( SHR) . Methods Twenty male SHR rats were randomly divided into the model group (group SHR) , ICS Ⅱ low ( ICS Ⅱ-L) , middle ( ICSⅡ-M) and high ( ICS Ⅱ-H) group, and male WKY rats were set as control group ( group WKY) . ICS Ⅱ-L, ICSⅡ-M and ICSⅡ-H groups were intragastrically administered with ICS Ⅱ for 12 weeks. After that the blood pressure was measured in rats. Then, the rats were sacrificed and the left ventricles were separated in order to calculate the left ventricular mass index. Mas-son staining was used to detect the occurrence of inter-stitial fibrosis in cardiac tissues. Real time PCR was used to observe the gene expression of MMP-2, MMP-9 and TIMP-1 in the left ventricle in SHRs. The protein expression levels of MMP-2, MMP-9, TIMP-1, Colla- gen Ⅰ and Collagen Ⅲ were measured by Western blot. Results Compared with SHR group, the myo-cardial fibrosis was reduced after ICS Ⅱ (8, 16 mg· kg-1) treatment. The blood pressure and left ventricu-lar mass index decreased(P<0.05). The expressions of MMP-2, MMP-9, CollagenⅠand CollagenⅢwere down-regulated in left ventricular tissues( P <0.05 ) , while the expression of TIMP-1 was up-regulated( P<0.05) . Conclusion Icariside Ⅱ ameliorates myocar-dial fibrosis in SHR, and the mechanisms might be re-lated to the decrease of blood pressure and down-regu-lation of MMP-2, MMP-9 expression and up-regulation of TIMP-1 expression.