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1.
Front Cardiovasc Med ; 9: 951704, 2022.
Article in English | MEDLINE | ID: mdl-36935650

ABSTRACT

Background: Fibrosis of the myocardium is one of the main pathological changes of adverse cardiac remodeling, which is associated with unsatisfactory outcomes in patients with heart disease. Further investigations into the precise molecular mechanisms of cardiac fibrosis are urgently required to seek alternative therapeutic strategies for individuals suffering from heart failure. SMOC2 has been shown to be essential to exert key pathophysiological roles in various physiological processes in vivo, possibly contributing to the pathogenesis of fibrosis. A study investigating the relationship between SMOC2 and myocardial fibrosis has yet to be conducted. Methods: Mice received a continuous ISO injection subcutaneously to induce cardiac fibrosis, and down-regulation of SMOC2 was achieved by adeno-associated virus-9 (AAV9)-mediated shRNA knockdown. Neonatal fibroblasts were separated and cultured in vitro with TGFß to trigger fibrosis and infected with either sh-SMOC2 or sh-RNA as a control. The role and mechanisms of SMOC2 in myocardial fibrosis were further examined and analyzed. Results: SMOC2 knockdown partially reversed cardiac functional impairment and cardiac fibrosis in vivo after 21 consecutive days of ISO injection. We further demonstrated that targeting SMOC2 expression effectively slowed down the trans-differentiation and collagen deposition of cardiac fibroblasts stimulated by TGFß. Mechanistically, targeting SMOC2 expression inhibited the induction of ILK and p38 in vivo and in vitro, and ILK overexpression increased p38 phosphorylation activity and compromised the protective effects of sh-SMOC2-mediated cardiac fibrosis. Conclusion: Therapeutic SMOC2 silencing alleviated cardiac fibrosis through inhibition of the ILK/p38 signaling, providing a preventative and control strategy for cardiac remodeling management in clinical practice.

2.
Herald of Medicine ; (12): 588-591,592, 2016.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-603522

ABSTRACT

Objective To investigate the effect of Shensong Yangxin capsule on cardiac remodelling of myocardial infarction mouse model and the possible molecular mechanisms. Methods Adult male C57BL/6J mice were divided into sham operation group(n=10), model control group(n=20)and Shensong Yangxin group(n=20)according to random number table. Left anterior descending branch of coronary artery was ligated to establish myocardic infarction model in the model control group and Shensong Yangxin group. From the 2nd day after the surgery, Shensong Yangxin ( 400 mg . kg-1 ) was intragastrically administered, and the death rate of the mice was observed.Four weeks after the surgery, echocardiography was used to measure the cardiac function;myocardiac infarction area was detected by pathological staining;the expression levels of cardiac remodelling markers and extracellular matrix proteins were detected by RT-PCR. The possible molecular mechanisms were screened by Western blotting. Results As compared with the model control group, Shensong Yangxin significantly reduced the mortality after myocardial infarction in mice(P<0.05), as well as the myocardial infarct size(P<0.05).The mRNA expression levels of cardiac remodelling markers ANP, BNP, and β-MHC and the extracellular matrix proteins(collagenⅠ, collagen Ⅲ, CTGF, TGFβ) decreased significantly in the Shensong Yangxin group as compared with the model control group. Western blotting showed that Shensong Yangxin significantly decreased activation of smad3, and reduced expression level of smad4. Conclusion Shensong Yangxin attenuates cardiac remodelling after myocardial infarction and the mechanism may be related with blockage of smad signaling pathway.

3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-464874

ABSTRACT

Objective:To explore expression of plasma omentin -1 in patients with central obesity (CO) complicated essential hypertension (EH) and its clinical significance .Methods : Serum level of omentin - 1 was measured by enzyme linked immunosorbent assay in 57 CO patients without EH (pure CO group) and 67 CO complicated EH patients (CO + EH group) ,and 56 healthy subjects (normal control group) .Blood glucose ,blood lipid and biochemical indexes were compared and analyzed among three groups ,and Logistic multi - factor gradual regression analysis was used to perform risk factor analysis .Results : Serum omentin - 1 level in CO + EH group was significantly lower than those of pure CO group and normal control group [ (25.15 ± 3.95) ng/ml vs .(45.63 ± 9.66) ng/ml ,(53.12 ± 7.97) ng/ml , P 0.05 ;Logistic multi - factor gradual regression analysis indicated that age and homeostasis model - insulin resistance index (HOMA - IR ) were independent risk factors affecting EH occurrence in obese people (OR = 1.124 ,95% CI : 1.000 - 1.248 ,P = 0.049 ;OR = 3.446 ,95% CI : 1.087 - 5.607 ,P = 0.001) ,while serum omentin - 1 level was an independent protective factor (OR = 0.423 ,95% CI : 0.210 - 0.636 , P = 0.001) .Conclusion : Serum omentin - 1 level may possess certain guiding significance in early diagnosis ,prevention and treatment for patients with central obesity complicated essential hypertension .

4.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-624080

ABSTRACT

The combination of lecturing and Problem-based Learning(PBL)teaching method is adopted in medical genetis. It is conducive to the development of self-directed learning skills, team skills,and problem-solving skills.

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