胸腺免疫抑制提取物对豚鼠支气管平滑肌的影响及平喘作用

目的：研究胸腺免疫抑制提取物（ｔｈｙｍｉｃｉｍｍｕｎｏｓｕｐｐｒｅｓｓｉｖｅｅｘｔｒａｃｔ，ＴＩＳＥ）对正常及致敏豚鼠支气管收缩的影响及平喘作用。方法：通过离体和整体实验，观察ＴＩＳＥ对以组胺和乙酰胆碱引起正常豚鼠支气管的收缩和以卵白蛋白诱发的致敏豚鼠支气管收缩的影响。结果：离体实验，ＴＩＳＥ７６０，３８０ｍｇ·Ｌ－１对组胺致正常豚鼠气管片的收缩具有对抗作用，对卵白蛋白所致的致敏豚鼠支气管平滑肌收缩有极显著的抑制作用（Ｐ＜０．０１），而对乙酰胆碱所致气管片收缩无明显影响；整体实验，ＴＩＳＥ２５，１８ｍｇ·ｋｇ－１可显著延长卵白蛋白所致的致敏豚鼠呼吸困难、抽搐和跌倒的潜伏期（Ｐ＜０．０１）。结论：ＴＩＳＥ能拮抗组胺刺激引起的正常豚鼠和卵白蛋白引起的致敏豚鼠离体气管片的收缩，抑制致敏豚鼠哮喘的发生。

胸腺免疫抑制提取物对Ⅰ型变态反应的影响

观察了胸腺免疫抑制提取物（１）对Ⅰ型变态反应的影响。结果表明，１用量８ｍｇ／ｋｇ以上能明显缩短大鼠被动皮肤过敏反应的蓝斑直径。还能抑制致敏豚鼠离体回肠平滑肌的过敏性收缩，其半数抑制浓度（ＩＣ５０）为４４６．７ｍｇ／Ｌ。

胸腺来源免疫抑制提取物对不同组织肿瘤细胞作用的研究

目的探讨小牛胸腺来源免疫抑制提取物 (TISE c)对不同组织来源肿瘤细胞的影响。方法采用3 H TdR掺入方法 ,检测TISE c对肝癌、肺腺癌、膀胱癌传代细胞株细胞增生的影响 ,以及在显微镜下观测TISE c对癌细胞形态学变化的影响。结果TISE c对 3种肿瘤细胞均具有抑制分裂增生作用 ,但是癌细胞形态正常。结论TISE c可能是一种能够抑制癌细胞分裂增生的生物制剂 ;对不同组织来源的癌细胞不存在组织特异性 ;

胸腺免疫抑制提取物对豚鼠支气管平滑肌的影响

目的:研究胸腺免疫抑制提取物(TISE)对正常及致敏豚鼠支气管收缩的影响及平喘作用。方法:通过离体和整体实验,观察TISE对组胺和乙酰胆碱引起正常豚鼠支气管的收缩和以卵白蛋白诱发的致敏豚鼠支气管收缩的影响。结果:离体实验,TISE760,380mg·L^(-1)对组胺致正常豚鼠气管片的收缩具有对抗作用,对卵白蛋白所致的致敏豚鼠支气管平湍肌收缩有极显著的抑制作用(P<0.01)。

Regulatory Action of Charred Gossamer Urocteae on the Functions of Mouse Oral Fibroblasts

Objective： To explore the influence of charred Gossamer urocteae （CGU） on the functions of primary cultured mouse oral fibroblasts and reveal its mechanism in wound healing. Methods： CGU was extracted with different solvents and ethanol extract （EE）, ethyl acetate fraction （EF）, n-butanol fraction （BF） and aqueous fraction （AF） were obtained. The effects of different fractions on the proliferation, matrix metaUoproteinase-2,9 （MMP-2,9） activities, synthesis of collagen and tissue inhibitor of metalloproteinase 1 （TIMP-1） in the mouse oral fibroblasts were determined by MTT, gelatin zymography, chloramine-T method, and enzyme-linked immunosorbent assay （ELISA） respectively. Results： EE, EF and BF at high concentrations could significantly inhibit proliferation of fibroblasts （P〈0.05 or P〈0.01）, and at low concentrations EF and BF could promote proliferation of fibroblasts, and BF and AF could significantly inhibit collagen synthesis （P〈0.05 or P〈0.01）. EE, EF and AF at high concentrations could significantly increase the MMP-9 activity, and BF and AF could significantly inhibit synthesis of TIMP-1. Conclusion： CGU at high concentrations can inhibit the proliferations of fibroblasts and synthesis of collagen, and in healing of wound, CGU at high concentrations possibly has the functions of anti-fibrosis and anti-scar, and the mechanism to promote degradation of collagen is possibly related to the increase in MMP-9 activity and the inhibition of TIMP-1 synthesis.