摘要
目的 从信号转导上探讨分叉双歧杆菌完整肽聚糖的抑瘤机制。方法 以结直肠癌裸鼠移植瘤为动物模型,用膜结合法、激光共聚焦显微镜和免疫组织化学法检测结直肠癌移植瘤和肿瘤对照组各20只BALB/c(nu/nu)裸鼠的蛋白酪氨酸激酶(PTK)和蛋白激酶C(PKC)α、βⅠ、βⅡ、γ、ε、ζ的活性以及核转录因子(NF)-κB的阳性细胞密度。结果 结直肠癌棵鼠移植瘤经完整肽聚糖处理后,其PTK活性和PKCα的平均荧光强度以及NF-κB的阳性细胞密度均显著低于肿瘤对照组(P<0.01);而PKCβⅠ、βⅡ、γ、ε和ζ的平均荧光强度在两组间则差异无显著性意义(P<0.01)。结论 分叉双歧杆菌的完整肽聚糖体内能明显降低结直肠癌PTK和PKCα的活性,同时阻止NF-κB的活化。
Objective To investigate the antitumor mechanisms of whole peptidoglycan(WPG) of bifidobaeteria bifidum in view of the signal transduction. Methods Nude mouse model of transplanted tumor of colorectal carcinoma was established and treated by intraperitoneal injection of WPG. The activity of protein tyrosine kinases(PTK), protein kinase C(PKC)α, βⅠ, βⅡ, γ, ε, ζ and the density of positive nuclear factor-κB(NF-κB) cell in transplanted tumors were measured. Results After treatment with WPG, the activity of PTK、average fluorescent strength of PKCα and density of positive NF-κB cell in transplanted tumors were significanfiy lower than those in untreatment control group(P<0.01). There was no difference in the average fluorescent strength of PKC βⅠ, βⅡ, γ, ε, ζ between the two groups (P>0.05). Conclusions WPG of bifidobacteria bifidum could markedly decrease the activity of PTK and PKCα, and inhibit the activation of NF-κB of colorectal in vivo.
出处
《中华胃肠外科杂志》
CAS
2003年第5期329-332,共4页
Chinese Journal of Gastrointestinal Surgery
基金
广东省自然科学基金(994066)
广东省深圳市科技局资助项目(200104077)