医学行业参考翻译范文

中医范文 西医范文 医疗器械范文

中医范文：

此范文为中译英

原文：

已知：衰老的发生是由众多因素所决定。自由基是多种因素之一，但因与其它学说有着直接或间接的关系，而成为诸多学说的中心。国内外研究表明：在代谢过程中D-半乳糖的长期作用可形成过量的超氧化阴离子自由基，其在对细胞膜不饱和脂肪酸的攻击中发生的过氧化反应，是发生亚急性衰老的根本原因，其衰老反应接近或相当于人体自然衰老。为此，本研究在文献报道基础上，通过与20月龄自然老化鼠的对比观察，证实：亚急性衰老模型鼠的退行性变化与20月龄自然生理性老化鼠特征的相近之处鲜明可见。2组均出现毛色暗淡，少有光泽，动作迟缓，反应不灵敏，体重增长率下降；肝、脑组织出现SOD活力下降，脂质过氧化物含量增高等血清酶学的老化特征。

西医学认为，衰老的表现特征主要在于：细胞体积缩小、数量减少和功能降低。已知，树突是神经元进行信息传递的重要结构。肝脏是机体集碳水化合物储存、代谢，激素灭活，血浆蛋白合成，类脂代谢调节以及药物和毒素解毒等多功能为一体的器官。为此，本研究将计测脑组织神经元与树突数量；正常肝细胞，双核肝细胞、肿胀肝细胞数目、肝组织小片坏死个数作为评价脑神经及肝组织细胞衰老程度的量化指标。结果显示：亚急性衰老模型鼠肝、脑组织结构出现与80周龄自然老化鼠相近的明显衰老特征。给予不同剂量人参养荣汤干预治疗后，脑细胞神经元数目接近正常，退行性变化明显改善；肝细胞增生、变性及坏死显著被抑制；其中以高剂量作用显著，并且具有显著的量效关系。

在明确人参养荣汤有效改善、延缓D-半乳糖所致亚急性衰老鼠肝、脑组织与细胞结构损伤的基础上，为探讨该方药延缓衰老组织细胞退行性改变与清除氧自由基能力、脂质过氧化状态，细胞损伤程度的相关性，选择血清SOD活性、MDA含量作为定量指标，旨在对该方药抗氧化作用给予客观地评价。

结果显示：中、高浓度人参养荣汤可显著改善早衰鼠血清SOD活性的下降，对抗脂质过氧化。

译文：

It has been known that occurrence of senescence is determined by multiple factors. Free radical is one of the factors, which has become the center of various theories for it is directly or indirectly related to other theories. Domestic and overseas researches have indicated that, the long-term effect of D-galactose in metabolic process may induce excess superoxidized radical anions, and then develop peroxidatic reactions when they attack unsaturated fatty acids in cellular membranes, which would be the basic reason for occurrence of subacute senescence. The senile reactions are closed to or equal to natural senescence of human bodies. Therefore, based on documents reports, through contrastive observation of 20-month-old natural senile mice, this study has confirmed that the anaplasia of subacute senile model mice was obviously similar to the features of 20-month-old naturally physiological senile mice. Mice in both two groups displayed dull color patterns, slow movements, insensitive responses and decrease of growth rates of body weight; hepatic and brain tissues in the mice presented senile features of sero-enzyme such as decrease in SOD activity, increase in content of lipid perhydrides and so on.

Western medicine considers that the main senile features are including deflation of cell volumes, decrease of cell number and decline of functions. It has been known that dendrites are the crucial structures for neuron to perform information transfer. Liver is the organ containing multiple functions including deposition and metabolism of carbohydrates, deactivation of hormones, synthesis of plasma proteins, metabolic regulation of adipoids as well as detoxication of drugs and toxins for organism. Therefore, this study would calculate and survey the following indexes as the quantitative indexes for evaluating the degrees of cell senescence in hepatic and brain tissues, including numbers of neurons and dendrites in brain tissues; numbers of normal hepatocytes, dikaryotic hepatocytes, swollen hepatocytes as well as flake necrosis. As the results shown, hepatic and brain tissues in subacute senile mice appeared similar senile features to those in 80-week-old natural senile mice. After administration of Panax Tonifying Soup Mix with different doses, the number of neurons in brain cells was approximate normal value, and the anaplasia was also notably improved; hepatocyte proliferation, degeneration and necrosis were evidently suppressed; the effects in high dose group were most remarkable; and noticeable dose-effect relationship was observed.

On the basis that Panax Tonifying Soup Mix can effectively improve and postpone cytoarchitecture impairment in hepatic and brain tissues in subacute senile mice, in order to approach the dependablity between postponing anaplasia of senile tissue cells and the ability of cleaning oxygen free radicals, lipid peroxidatic conditions, degree of cell injury of the recipe-medicine, serum SOD activity and MDA content were selected as quantitative indexes for objectively evaluating the antioxidation of this recipe-medicine.

As shown in results, moderate and high doses of Panax Tonifying Soup Mix can obviously improve the decrease of serum SOD activity and against lipid peroxidation in presenile mice.