Myocardial apoptosis is an important pathologic basis of ischemia-reperfusion injury (I/R). Transforming growth factor β1 (TGFβ1) participates in the regulation of oxidative damage and apoptosis. TGFβ1 is upregulated in the repair process of I/R injury. It is speculated that TGFβ1 over-expression is involved in the endogenous protective mechanism of I/R injury. This study explores the significance of TGFβ1 in myocardial cell apoptosis after I/R.Rat myocardial I/R injury model was established. Left ventricular ejection fraction (LVEF) and Left ventricular fractional shortening (LVFS) were detected by ultrasonic cardiogram. TGFβ1 expression in the myocardium was tested. H9C2 cells were cultured under ischemic hypoxic condition for 6 h, and then were treated by reoxygenation for 6 h to simulate I/R model. H9C2 cells were divided into three groups, including I/R+pIRES2-Blank, I/R+pIRES2 TGFβ1, and I/R+pIRES2-TGFβ1+LY364947. TGFβ1 mRNA and protein levels were evaluated. Cell apoptosis and reactive oxygen species (ROS) were determined by flow cytometry.LVEF and LVFS significantly decreased in I/R group compared with Sham group. TGFβ1 mRNA and protein expressions in myocardium from I/R group up-regulated than the control. I/R treatment markedly elevated TGFβ1 mRNA and protein levels, increased ROS content, and enhanced cell apoptosis in H9C2 cells. Over-expression of TGFβ1 significantly weakened ROS production and apoptosis in H9C2 cells after I/R. TGFβ receptor inhibitor LY364947 restrained ROS production and apoptosis attenuation in H9C2 cells treated by TGFβ.TGFβ1 alleviates myocardial cell apoptosis after I/R. Blocking TGFβ1 attenuates the protective effect of TGFβ1 on I/R injury.
Ischemia/reperfusion (I/R) injury is associated with substantial clinical implications, including a wide range of organs such as the brain, kidneys, lungs, heart, and many others. I/R injury (IRI) occurs due to the tissue injury following the reestablishment of blood supply to ischemic tissues, leading to enhanced aseptic inflammation and stimulation of oxidative stress via reactive oxygen and nitrogen species (ROS/RNS). Since ROS causes membrane lipids’ peroxidation, triggers loss of membrane i...
Last. Long Ma(First Affiliated Hospital of Xinjiang Medical University)
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Nuclear receptor subfamily 4, group A, member 1 (NR4A1) can aggravate ischaemia-reperfusion (I/R) injury in the heart, kidney and brain. Thus, the present study aimed to unravel the role of NR4A1 on hepatic I/R injury. For this purpose, the mouse hepatic I/R model and H/R-exposed mouse hepatocytes model were established to stimulate the hepatic and hepatocellular damage. Then, the levels of ALT and AST as well as TNF-α and IL-1β expression were measured in the mouse serum and supernatant of hepa...
Abstract Objective Dimethyl fumarate (DMFU), a known Nrf2 activator, has proven its positive effect in different organs against ischemia/reperfusion (Is/Re) injury. Nevertheless, its possible impact to modulate intestinal Is/Re-induced injury has not been previously demonstrated before. Hence, this study aimed to investigate DMFU mechanistic maneuver against intestinal Is/Re. Methods To accomplish this goal, Wistar rats were allocated into four groups; Sham-operated (SOP), intestinal Is/Re (1 h/...
Mitochondria are double-membrane cellular organelles that can provide the required energy and metabolic intermediates to cardiomyocytes. Mitochondrial respiratory chain defects, structure abnormalities, and DNA mutations, as well as other mitochondria-related factors, can affect the normal function of cardiomyocytes, causing an imbalance in intracellular calcium ion homeostasis, production of reactive oxygen species, apoptosis, and other cellular and subcellular events. Mitochondrial quality con...
Last. Qilin Ma(CSU: Central South University)H-Index: 1
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Myocardial ischemia/reperfusion (I/R) injury contributes to the pathogenesis of numerous diseases. Based on its antioxidant and anti‑inflammatory effects, dimethyl fumarate (DMF) has been reported to exert protective effects against I/R. However, to the best of our knowledge, its potential role as a myocardial protective agent in heart disease has received little attention. Previous studies have suggested that DMF may exert its protective effects by activating nuclear factor erythroid 2‑related ...
Gastrodin (GAS) is the major component isolated from the rhizome of the Chinese traditional medicinal herb “Tianma.” Many clinical studies have found that GAS protects cardiomyocytes in cardiovascular diseases, although the effects and underlying mechanisms on cardiovascular anoxia/reoxygenation (A/R) injury remain unknown. This study is aimed at exploring the effect of gastrodin on cardiomyocytes in A/R injury. Our results suggested that the protective effect of GAS on cardiomyocytes is associa...
Background Chronic intermittent hypoxia (CIH), an important basis of the pathogenesis of organ damage induced by obstructive sleep apnea syndrome (OSAS), is associated with myocardial injury, such as left ventricular dysfunction, apoptosis, and oxidative stress. Endogenous hydrogen sulfide (H2S) plays an important role in maintaining cardiovascular functions. Many studies have demonstrated that exogenous H2S has protective effects against myocardial injury induced by various cardiovascular disea...
#1Weiwei Wei(HUST: Huazhong University of Science and Technology)H-Index: 1
#2Chao Wang(HUST: Huazhong University of Science and Technology)H-Index: 1
Last. Dongjian Li(HUST: Huazhong University of Science and Technology)H-Index: 1
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: The purpose of this study is to investigate the content of hydrogen sulfide (H2S) in plasma of cirrhosis rats combined with portal hypertension and the correlation with indexes of liver function and liver fibrosis. Thirty female Sprague-Dawley rats were randomly divided into normal control group (NC), liver cirrhosis group (LC) and cirrhosis + propargylglycine (PPG) group (LC+PPG). Cirrhosis and portal hypertension were induced by carbon tetrachloride. Rats in LC+PPG group were intraperitoneal...