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Question

GPs100μg/ml也能对抗美蓝（Mb）所致血管环舒张功能损伤的作用。血管内皮能释放前列环素（PGI2）和内皮衍生松弛因子（EDRF）等调节血管张力和增强自身抗损伤能力，OFR所致血管舒张能力降低与内皮释放EDRF减少有关，GPs能对抗因Mb抑制EDRF所致血管舒张功能降低，GPs可能保护EDRF活性。GPs的作用可被INDO阻断，表明GPs作用可能通过促进组织释放PGI2进而抗膜脂质过氧化有关，可减少人中性白细胞内超氧阴离子和过氧化氢含量；对人单核细胞和鼠巨噬细胞，GPs可减少酵母多糖触发的化学发光性氧化爆发；对于Fe2+半胱氨酸、抗坏血酸-NADPH或过氧化氢在肝微粒体和血管内皮细胞产生的LPO增加，GPs可抑制这作用，由于氧化损伤而减少了的肝微粒体和浅粒体的膜流动性，GPs可逆转，增加血管内皮细胞线粒体酶活性。减少这些细胞内乳酸脱氢酶的泄漏，提示GPs可保护生物膜免受氧化损伤，GPs的这些广泛的抗氧化效果对多种疾病如动脉粥祥硬化、肝病和炎症的预防和治疗均可有定价。有人指出脂质过氧化作用可使脂质含量较高的生物膜组成发生变化，且使DNA，RNA结构受到损害，引起蛋白质分子的交联，导致细胞的衰老，绞股蓝显著降低LPO的作用值得重视。绞股蓝能抑制脂肪细胞产生游离脂肪酸及合成中性脂肪。用大鼠附睾的脂肪组织制备脂肪细胞进行培养，在培养液中加ACTH或肾上腺素可使脂肪细胞分解而产生游离脂肪酸，如同时添加GPs则减少游离脂肪酸的生成量达28%左右。以脂肪细胞和示踪化合物14C-葡萄糖在37℃共同培育30分钟，测定脂肪细胞的每分钟脉冲数（CPM）作为葡萄糖进入细胞合成为中性指防的指标，培养液添加GPs后，每克脂肪细胞测得的CPM数仅为未加GPs组的50%左右。

Answer 1

GPs100 μ g/ml can also fight methylene blue (Mb) induced vascular ring diastolic function injury.Vascular endothelial release of prostacyclin (PGI2) and endothelial derived relaxing factor (EDRF) and the regulation of vascular tone and strengthen its anti-damage ability, OFR induced vasodilatation capacity decreases with the decrease of endothelial EDRF release, GPs can antagonize the inhibition of EDRF by Mb induced vasodilation in lower EDRF activity, GPs may protect.The effect of GPs could be inhibited by INDO, showed that the GPs effect may be through the promotion of tissue release PGI2 and anti lipid peroxidation, reduces human neutrophil intracellular superoxide anion and hydrogen peroxide content; on human monocytes and macrophages in rats, GPs can decrease yeast polysaccharide triggered chemiluminescence oxidative burst; for Fe2+ cysteine -NADPH, ascorbic acid or hydrogen peroxide in liver microsomes and vascular endothelial cells produce LPO increased, GPs can inhibit this effect, due to oxidative damage and reduced liver microsomes and shallow bulk membrane fluidity, GPs can be reversed, increased vascular endothelial cell mitochondria enzyme activity.Reduction of these intracellular lactate dehydrogenase leakage, suggesting that GPs may protect the membrane from oxidative damage, GPs these broad antioxidant effect on various diseases such as arterial congee Xiang hardening, the prevention and treatment of liver disease and inflammation may have pricing.It is pointed out that lipid peroxidation may cause higher content of biological membrane lipid composition changes, and that the DNA, RNA structure damage, caused by protein cross-linking, resulting in cell senescence, Gynostemma pentaphyllum significantly reduced LPO role worthy of attention.Gynostemma pentaphyllum can inhibit fat cells produce free fatty acids and synthesis of neutral fat.Using a rat epididymal adipose tissue preparation of fatty cells were cultured in the medium with ACTH, or epinephrine to the decomposition of fat cells and produce free fatty acids, such as adding GPs reduction of free fatty acid production reached about 28%.In fat cells and tracer compounds 14C- glucose at 37 ℃ fostered 30 minutes, the determination of fat cell pulses per minute (CPM) as the glucose into the cells for synthesis of neutral point to defend the index, medium after adding GPs, per gram of fat cells measured CPM number is only about 50% without GPs group.

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Answer 2

GPs100 μg/ml can also fight methylene blue (Mb ) induced vascular ring diastolic function injury. Vascular endothelial release of prostacyclin ( PGI2) and endothelial derived relaxing factor ( EDRF ) and the regulation of vascular tone and strengthen its anti-damage ability, OFR induced vasodilatation capacity decreases with the decrease of endothelial EDRF release, GPs can antagonize the inhibition of EDRF by Mb induced vasodilation in lower EDRF activity, GPs may protect. The effect of GPs could be inhibited by INDO, showed that the GPs effect may be through the promotion of tissue release PGI2and anti lipid peroxidation, reduces human neutrophil intracellular superoxide anion and hydrogen peroxide content; on human monocytes and macrophages in rats, GPs can decrease yeast polysaccharide triggered chemiluminescence oxidative burst; for Fe2+ cysteine -NADPH, ascorbic acid or hydrogen peroxide in liver microsomes and vascular endothelial cells produce LPO increased, GPs can inhibit this effect, due to oxidative damage and reduced liver microsomes and shallow bulk membrane fluidity, GPs can be reversed, increased vascular endothelial cell mitochondria enzyme activity. Reduction of these intracellular lactate dehydrogenase leakage, suggesting that GPs may protect the membrane from oxidative damage, GPs these broad antioxidant effect on various diseases such as arterial congee Xiang hardening, the prevention and treatment of liver disease and inflammation may have pricing. It is pointed out that lipid peroxidation may cause higher content of biological membrane lipid composition changes, and that the DNA, RNA structure damage, caused by protein cross-linking, resulting in cell senescence, Gynostemma pentaphyllum significantly reduced LPO role worthy of attention. Gynostemma pentaphyllum can inhibit fat cells produce free fatty acids and synthesis of neutral fat. Using a rat epididymal adipose tissue preparation of fatty cells were cultured in the medium with ACTH, or epinephrine to the decomposition of fat cells and produce free fatty acids, such as adding GPs reduction of free fatty acid production reached about 28%. In fat cells and tracer compounds14C- glucose at 37 ℃fostered30 minutes, the determination of fat cell pulses per minute ( CPM ) as the glucose into the cells for synthesis of neutral point to defend the index, medium after adding GPs, per gram of fat cells measured CPM number is only about 50% without GPs group.祝成功，望采，谢谢！！！！！！！！！！！！！！！！