几种胶原酶抑制剂滴眼液的效果比较

目的 观察比较 6种眼科外用药物 ,为临床筛选较强的抑制胶原酶的眼液。方法用鼠胶原、胶原酶及考马斯亮蓝比色法来检测药物抑制胶原酶的能力。结果 6种药物有不同程度抑制胶原酶作用 ,其中卡托普利极强、乙酰半胱氨酸和依地酸钠较强 ,而枸橼酸钠、硫代硫酸钠和四环素较差。结论 0 .5 g· L- 1卡托普利眼液抑制胶原酶能力极强、副作用小、刺激性极微。

Ⅳ型胶原酶及其抑制剂在抗肿瘤研究中的进展

作为基质金属蛋白酶家族成员的Ⅳ型胶原酶,除参与多种正常的生理功能外,还在肿瘤的发生发展过程中发挥着重要作用,与肿瘤的血管生成,肿瘤的侵袭和转移密切关联.研究发现有一些Ⅳ型胶原酶抑制剂能够通过抑制其酶活性,从而减缓肿瘤发展,这些抑制剂包括天然物质、人工合成物质及抗体类物质.目前,人们正利用抗体抑制剂进行抗肿瘤作用的研究,研发新型抗癌药物.

卡托普利预处理对自酸蚀粘接剂牙本质粘接持久性的影响

目的:通过卡托普利抑制金属基质蛋白酶的活性以提高粘接界面的稳定性。方法:采用不同浓度的卡托普利乙醇溶液和卡托普利乙醇/水溶液对人离体牙牙本质表面进行预处理,通过场发射扫描电镜观察卡托普利预处理对牙本质表面形貌的影响;在此基础上通过两种自酸蚀粘接剂对牙本质进行粘接,表征即刻粘接强度,并通过老化处理,评价卡托普利预处理对粘接持久性的影响。结果:扫描电镜结果提示,卡托普利溶液可以部分去除沾污层并暴露牙本质胶原。基于扫描电镜结果,选择0.15 g/m L卡托普利乙醇溶液(50%乙醇)处理30 s作为预处理条件,通过可乐丽菲露SE BOND进行牙本质粘接,即刻微拉伸强度从(30.80±4.70)MPa提升至(37.48±3.20)MPa(P<0.05);老化处理1年后,对照组微拉伸强度显著下降[(22.90±6.82)MPa,P<0.05],而实验组微拉伸强度没有明显的变化[(36.56±5.10)MPa,P>0.05]。用可乐丽菲露S3BOND进行牙本质粘接,对照组的即刻微拉伸强度为(31.33±4.11)MPa,与实验组(34.70±4.07)MPa差异无统计学意义(P>0.05);老化处理1年后,实验组的微拉伸强度高于对照组[分别为(32.36±3.58)MPa和(21.43±6.27)MPa,P<0.05]。结论:卡托普利预处理不仅可以提高自酸蚀粘接的即刻粘接强度,而且改善了粘接的持久性。

Effects of fibril- or fixed-collagen on matrix metalloproteinase-1 and tissue inhibitor of matrix metalloproteinase-1 production in the human hepatocyte cell line HLE

AIM:Matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) are central to the spontaneous resolution of liver fibrosis. The mechanisms involved have been investigated in hepatic stellate cells (HSC), but not in hepatocytes. We investigated the effects of fibril- and fixed-collagen on MMP-1 and TIMP-1 production in hepatocytes, using the HLE cell line. METHODS: Fibril type I and IV collagen were prepared by HCI digestion of type I and IV collagen, respectively. For fixed-collagen, culture dishes were coated with fibril type I or IV collagen and fixed by ultraviolet. Type I collagenase activity was measured using fluorescein isothiocyanate-labeled type I collagen. MMP-1 and TIMP-1 in HLE cells were measured by a one-step sandwich enzyme immunoassay. RESULTS: Both fibril type I and IV collagen significantly increased type I collagenase activity about two-fold compared with no fibril collagen. The effects of the fibril collagen were not affected by the coating condition. There was no significant difference in the effects on collagenase activity between cells cultured in medium containing fibril type I collagen and those cultured in the presence of type IV collagen. Both types of fibril collagen significantly increased MMP-1 production, and showed more than 10-fold higher levels of MMP-1 than the control. The enhanced MMP-1 production by fibril collagens was unaffected by the coating condition. By contrast, TIMP-1 production was not changed by the addition of fibril type I or IV collagen, and neither was it affected by the coating conditions. Coating with type I collagen significantly suppressed MMP-1 production by almost one-tenth compared with no coating. By contrast, TIMP-1 production was not affected by either the absence of a collagen coat or by increasing the concentration of the coating collagen. CONCLUSION: These results indicated that, in HLE cells, fibril- and fixed-collagen have opposite effects on MMP-1 production without affecting TIMP production. Fibril collagen induced collagenase activity by up-regulation of MMP-1 production without affecting TIMP-1 production. By contrast, fixed collagen reduced MMP-1 production. Our results suggest that hepatocytes might also play an important role in the regulation of the hepatic fibrosis alongside HSC.

促进成纤维细胞生长的余甘子提取物

用MTT还原方法评价余甘子提取物对皮肤真皮成纤维细胞生长的促进作用。结果表明：余甘子提取物具有成纤维细胞增殖作用，从而证实了其对成纤维细胞生长的促进作用，为透明质酸酶抑制剂、胶原酶抑制剂、酪氨酸酶抑制剂、黑色素产生抑制剂、弹性酶抑制剂和Maillard反应抑制剂。该提取物具有缓泻、镇痛、抗炎、促智、降糖、杀病毒、抗微生物等活性，可用于药品、准药品、化妆品、食品；加工成片剂、胶囊、颗粒、半固体、凝胶、液剂、粉末、乳剂、分散剂、安瓿剂等；用来治疗便秘、尿痛、呕吐、灼热，降糖、降血清胆固醇、保肝、提高记忆、调节免疫等。