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一、本实验以大剂量醋酸氢化可的松使动物引起一系列的耗竭现象,达到虚损状态,似可比拟祖国医学的“阳虚”。虚损现象表现为:动物死亡较多、体重较减轻、拱背少动、反应迟钝,体毛不荣。内脏器官如肝、脾等也有明显变化:肝细胞显著膨大,核酸减少,琥珀酸脱氢酶活性降低,糖元增加,枯氏细胞减少;脾脏体积显著缩小,其淋巴细胞及淋巴细胞的核酸含量减少。助阳药对醋酸氢化可的松引起的“阳虚”现象,似有调节作用:阳虚组动物肝、脾的核酸含量降低,肝细胞琥珀酸脱氢酶的活性下降,加服助阳药后,肝、脾核酸含量上升,肝细胞琥珀酸脱氢酶活性上升。阳虚动物肝糖元含量增加,服助阳药后肝糖元含量下降。助阳药并对阳虚动物的肝细胞、枯氏细胞及脾脏的淋巴细胞有保护作用。二、本实验还以分子生物学水平研究阴虚造型及几种滋阴药的作用,以氚标记胸腺嘧啶脱氧核苷及尿嘧啶注射实验动物,提取肝、脾的脱氢核糖核酸及核糖核酸,并进行了肝糖元组织化学与痛阈的研究。以甲状腺素及利血平造成的小白鼠动物模型,似可比拟为阴虚症。在实验6天,动物表现为体重减轻,躁动不安,痛阈下降,肝、脾核酸合成上升;实验8及10天,大部分动物非常瘦小,行动迟缓,肝脏核酸合成下降。动物的肝糖元均下降。滋阴中药对阴虚动物的虚证似有调节作用:肝、脾核酸合成升高时可以使之降低,肝脏核酸合成降低时可以使之升高,使降低的肝糖元上升,也可使降低的痛阈上升。
1. In this experiment, a large dose of hydrocortisone acetate caused the animal to cause a series of depletion phenomena, reaching a state of catastrophic loss, which may be comparable to the “yang deficiency” of the motherland medicine. The phenomenon of catastrophic loss is manifested as: more animal deaths, less weight, less movement of the arches, unresponsiveness, and poor body hair. Visceral organs such as liver and spleen also have significant changes: hepatocytes are significantly enlarged, nucleic acid is reduced, succinate dehydrogenase activity is decreased, glycogen is increased, Kupffer cells are decreased, spleen volume is significantly reduced, and the nucleic acid content of lymphocytes and lymphocytes is reduced. cut back. The “yang-deficiency” phenomenon caused by hydrocortisone acetate may have a regulatory effect on Yangyang medicine: the nucleic acid content of the liver and spleen of Yang deficiency group animals is decreased, and the activity of succinate dehydrogenase in liver cells is decreased, and the auxiliary medicine is added. After that, the liver and spleen nucleic acid content increased, and the activity of succinate dehydrogenase in liver cells increased. The content of hepatic glycogen in animals with yang deficiency increased, and the content of hepatic glycogen decreased after taking yang. Yangyang drugs have protective effects on hepatocytes, churn cells and spleen lymphocytes of animals with yang deficiency. Second, the experiment also studied the role of yin deficiency modeling and several nourishing yin drugs at the molecular biology level. The thymidine and uracil were injected into experimental animals with guanidine to extract dehydroribonucleic acid and ribonucleic acid from the liver and spleen. , and conducted liver glycogen histochemistry and pain threshold research. The mouse model caused by thyroxine and reserpine may be comparable to yin deficiency syndrome. On day 6 of the experiment, the animals showed weight loss, restlessness, decreased pain threshold, and increased nucleic acid synthesis in the liver and spleen; in the 8th and 10th days of the experiment, most animals were very thin and sluggish, and the liver nucleic acid synthesis decreased. The animals’ liver glycogen declined. Ziyin Chinese medicine seems to have a regulating effect on the deficiency of yin and deficiency animals: when the synthesis of liver and spleen nucleic acid is elevated, it can be reduced. When the synthesis of liver nucleic acid is reduced, it can be increased, so that the decreased hepatic glycogen can be increased. The reduced pain threshold rises.