机构地区:[1]内蒙古医科大学药学院,呼和浩特010110 [2]内蒙古医科大学基础医学院,呼和浩特010110 [3]内蒙古医科大学新药临床前安全评价中心,呼和浩特010110 [4]内蒙古医科大学蒙医药研究院,呼和浩特010110
出 处:《中华中医药杂志》2016年第12期5232-5236,共5页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:内蒙古医科大学"科技百万工程"项目(No.YKD2012KJBW007);内蒙古自治区自然科学基金项目(No.2013MS1211)~~
摘 要:目的:探讨蒙药寒水石化灰小剂对S-180荷瘤小鼠肿瘤生长的影响及凋亡相关蛋白的调控作用。方法:建立S-180荷瘤小鼠模型,随机分为模型组,阳性对照组,环磷酰胺+寒水石化灰小剂低剂量联合给药组,寒水石化灰小剂高、中、低剂量组。各组连续给药后,称瘤重、脾重,计算抑瘤率、脾系数;ELISA法检测血清中免疫相关因子TNF-α、IL-6、IL-10的含量;取肿瘤组织常规HE染色镜下观察肿瘤组织;应用Western Blot方法检测凋亡相关蛋白Bcl-2、Bax和血管内皮细胞标志物CD34的表达。结果:与模型组相比,各给药组的瘤重均显著降低,抑瘤率分别为阳性对照组50.28%,联合给药组54.73%,寒水石化灰小剂高、中、低剂量组分别为31.07%、36.05%、13.14%。联合给药组和寒水石化灰小剂高、中剂量组IL-6含量均显著高于模型组和阳性对照组;联合给药组和寒水石化灰小剂高、中剂量组IL-10含量均显著低于模型组(P<0.05,P<0.01)。模型组病理切片观察发现模型组肿瘤组织血管丰富,坏死率约为10%-15%,联合给药组,寒水石化灰小剂高、中剂量给药组血管相对较少,纤维化明显,坏死率明显高于模型组;肿瘤组织的Bcl-2蛋白表达显著降低,而Bax蛋白表达显著增加,Bcl-2/Bax比值显著降低(P<0.05)。结论:寒水石化灰小剂可能是通过调节免疫,调控凋亡相关蛋白的表达,抑制肿瘤血管生成相关蛋白表达,发挥抑制肿瘤生长的作用;同时,寒水石化灰小剂与环磷酰胺有协同抗肿瘤作用。Objective: To study the effect of Calcitum Ashing Agent in inhibiting tumor and regulating apoptin. Methods: S-180 tumor-bearing mice were randomly divided into tumor-bearing model group, cyclophosphamide positive group, cyclophosphamide combined with Calcitum Ashing Agentt low dose group, and Calcitum Ashing Agent high, medium and low dose group. After the medication, body, spleen and tumor tissue weight were measured and inhibition rate, index of spleen of each group were calculated. ELISA was used to examine the content of TNF-α, IL-6, IL-10. The tumor tissues were observed by HE staining, and Western Blot was used to detect apoptosis-related protein Bcl-2, Bax and vascular endothelial cell marker CD34 expression in tissue. Results: Compared with the tumor-bearing model group, the other groups showed higher tumor inhibition rates, for instance 50.28% for the cyclophosphamide positive group, 54.73% for the co-administration group, and 31.07%, 36.05%, 13.14% for the Calcitum Ashing Agent high, medium and low dose group. The content of IL-6 in co-administration group andthe Calcitum Ashing Agent high, medium dose group were higher than the model and the cyclophosphamide group, as well as the content of IL-10 were lower than model group, with statistical difference(P〈0.05, P〈0.01). Pathological results showed that blood vessels of tumor tissue were rich and necrosis rate was about 10%-15% in model group, but there were less vessels, obvious fibrosis, higher necrosis rate in the co-administration group and the Calcitum Ashing Agent high, medium dose group. The expression of protein Bcl-2, Bax in tissue showed that Bcl-2 decreased, Bax increased, and Bcl-2/Bax ratio decreased, with statistically significant difference(P〈0.05, P〈0.01). Conclusion: Calcitum Ashing Agent can inhibite the growth of tumor by regulating the immune, regulating the expression of apoptin and inhibiting the expression of tumor angiogenesis related protein. Besides, Calcitum Ashing Agent and cyclophosphamide have syner
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