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Your search keyword '"Ma, Lei-Lei"' showing total 42 results
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42 results on '"Ma, Lei-Lei"'

2. Hypertrophic preconditioning attenuates post-myocardial infarction injury through deacetylation of isocitrate dehydrogenase 2

Author

Ma, Lei-lei, Kong, Fei-juan, Ma, Yuan-ji, Guo, Jun-jie, Wang, Shi-jun, Dong, Zheng, Sun, Ai-jun, Zou, Yun-zeng, and Ge, Jun-bo

Abstract

Ischemic preconditioning induced by brief periods of coronary occlusion and reperfusion protects the heart from a subsequent prolonged ischemic insult. In this study we investigated whether a short-term nonischemic stimulation of hypertrophy renders the heart resistant to subsequent ischemic injury. Male mice were subjected to transient transverse aortic constriction (TAC) for 3 days followed aortic debanding on D4 (T3D4), as well as ligation of the left coronary artery to induce myocardial infarction (MI). The TAC preconditioning mice showed markedly improved contractile function and significantly reduced myocardial fibrotic area and apoptosis following MI. We revealed that TAC preconditioning significantly reduced MI-induced oxidative stress, evidenced by increased NADPH/NADP ratio and GSH/GSSG ratio, as well as decreased mitochondrial ROS production. Furthermore, TAC preconditioning significantly increased the expression and activity of SIRT3 protein following MI. Cardiac-specific overexpression of SIRT3 gene through in vivo AAV-SIRT3 transfection partially mimicked the protective effects of TAC preconditioning, whereas genetic ablation of SIRT3 in mice blocked the protective effects of TAC preconditioning. Moreover, expression of an IDH2 mutant mimicking deacetylation (IDH2 K413R) in cardiomyocytes promoted myocardial IDH2 activation, quenched mitochondrial reactive oxygen species (ROS), and alleviated post-MI injury, whereas expression of an acetylation mimic (IDH2 K413Q) in cardiomyocytes inactivated IDH2, exacerbated mitochondrial ROS overload, and aggravated post-MI injury. In conclusion, this study identifies TAC preconditioning as a novel strategy for induction of an endogenous self-defensive and cardioprotective mechanism against cardiac injury. Therapeutic strategies targeting IDH2 are promising treatment approaches for cardiac ischemic injury.

Published
2024
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41. [Sevoflurane preconditioning produces delayed cardioprotection effect through up-regulation of inducible nitric oxide synthase in rats].

Author

Ma LL, Zhang FJ, and Yan M

Subjects
Anesthetics, Inhalation pharmacology, Animals, Disease Models, Animal, Male, Myocardial Reperfusion Injury enzymology, Myocardial Reperfusion Injury pathology, Myocardium enzymology, Myocardium pathology, Rats, Rats, Sprague-Dawley, Sevoflurane, Up-Regulation drug effects, Ischemic Preconditioning, Myocardial, Methyl Ethers pharmacology, Myocardial Reperfusion Injury prevention & control, Nitric Oxide Synthase Type II metabolism
Abstract

Objective: To investigate whether inhaled sevoflurane is capable of producing delayed cardioprotection effect in rats and its underlying mechanisms., Methods: Male Sprague-Dawley rats inhaled 1.0 minimum alveolar concentration (MAC) sevoflurane, 1.5 MAC sevoflurane,or O(2) for 1 h. After 24 h and 48 h the left coronary artery of rats was occluded for 30 min,followed by 120 min of reperfusion. Hemodynamics was continuously recorded and myocardial infarct size was determined by Evans blue and triphenyltetrazolium chloride staining. The expression of nitric oxide synthase (NOS) was assessed by immunoblotting., Results: 1.0 MAC sevoflurane and 1.5 MAC sevoflurane improved cardiac pump function after reperfusion and reduced myocardial infarct size with the increased iNOS expression (P<0.05). However,the expression of eNOS and p-eNOS was not affected (P>0.05). A selective iNOS inhibitor 1400 W abolished the cardioprotection effect induced by inhalation of 1.0 MAC sevoflurane for 24 h., Conclusion: Sevoflurane produces delayed cardioprotection through the up-regulation of iNOS expression.

Published
2012

42. [Preparation of tanshinone microemulsion and its absorption in rat intestine in situ].

Author

Li HL, Zhang ZY, Ma LL, and Chen XY

Subjects
Abietanes, Animals, Emulsions, Male, Particle Size, Phenanthrenes administration & dosage, Phenanthrenes isolation & purification, Plants, Medicinal chemistry, Rats, Rats, Sprague-Dawley, Technology, Pharmaceutical methods, Intestinal Absorption, Intestine, Small metabolism, Phenanthrenes pharmacokinetics, Salvia miltiorrhiza chemistry
Abstract

Objective: To prepare tanshinone microemulsion (Tan-ME) and investigate its properities and the absorption character in rat intestine in situ., Method: The microemulsions were prepared and characterized using Zetapals Zeta potential/particle size analysis and atomic force microscope. A HPLC method for determination of tanshinone IIA in the intestinal flux was established. RESUILT: The Tan-ME was fine droplet with an average droplet size of (32.25 +/- 6.59) nm. The results of Tan-ME absorption in small intestinal indicated that Tan-ME could improve the absorption of tanshinone IIA in rat small intestine, but the absorption coefficient of Tan-ME, Ka was influenced by the ratio of water-phase in Tan-ME., Conclusion: Tan-ME could improve the absorption of tanshinone IIA in rat small intestine. Thus bioavailability of tanshinone was improved.

Published
2007

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