Shu-long Yang

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BACKGROUND L-Arginine has been described as a potential immunostimulant in vitro and in vivo. Excessive arginine, however, may be counterproductive. Data support the concept of minimal arginine requirements for normal lymphocyte proliferation, but the results of supplementation with pharmacologic doses of arginine have been contradictory. We hypothesized(More)
BACKGROUND Hepatic ischemia-reperfusion (I/R) injury is an important clinical issue and relates to cysteinyl leukotrienes (LTs), the first committed synthesis step of which is that LTC4 synthesis enzymes including leukotriene C4 synthase (LTC4S), microsomal glutathione-S-transferase (mGST)2, and mGST3-catalyzed LTA4 and reduced glutathione (GSH), to(More)
The effects of NO on LTC4 generation during hepatic ischemia-reperfusion (I/R) are largely unclear. Sprague-Dawley rats were divided into control, I/R and sodium nitroprusside (SNP, 2.5, 5 and 10 microg/kg/min)+I/R groups. Liver was subjected to I/R injury, saline or SNP administered intravenously. The protein expressions of LTC4 synthesis enzymes including(More)
Leukotriene (LT) C4 (LTC4) synthesis enzymes including LTC4 synthase (LTC4S), microsomal glutathione S-transferase (MGST) 2 and MGST3 can all conjugate LTA4 and reduced glutathione (GSH) to form LTC4, which is related to hepatic ischemia/reperfusion (I/R) injury. The relationship between nitric oxide (NO) and cysteinyl LTs has been shown in previous(More)
OBJECTIVE To investigate the interaction between opioid receptor (OR) stimulation and adrenergic receptor (AR) stimulation in the isolated ischaemia/reperfusion (I-R) rat heart. METHODS Male Sprague-Dawley rats were used for Langendoff isolated heart perfusion. Myocardial ischemia for 20 min was followed by 30 min of reperfusion, during which the kappa-OR(More)
Hepatic ischemia reperfusion injury (HIRI) is a clinical condition which may lead to cellular injury and organ dysfunction. The role of nitric oxide (NO) in HIRI is complicated and inconclusive. NO produced by endothelial nitric oxide synthase (eNOS) activation plays a protective role during early HIRI. But eNOS overexpression and the resulting excessive NO(More)
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