2型糖尿病对舌发育不良及p16相关衰老过程影响的实验研究

E. Altun, H. Yazici, E. Arslan, K. G. Tulaci, H. Erken
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引用次数: 3

摘要

目的探讨链脲佐菌素诱导的实验性糖尿病对大鼠舌组织p16、p53、Ki67、Bcl2表达及组织病理学改变的影响。材料与方法选用成年雌性Sprague-Dawley大鼠22只。将大鼠随机分为2组(n = 14),分别为对照组(n = 8)和糖尿病组(n = 6)。DM组大鼠单次腹腔注射链脲佐菌素诱导糖尿病。使用福尔马林固定和石蜡包埋的舌组织切片进行组织病理学和免疫组织化学评价。结果DM组与对照组在上皮厚度、丝状乳头长度、丝状乳头宽度方面差异均有统计学意义(p = 0.005、p = 0.001、p = 0.006)。各组间单核炎性细胞浸润、毛细血管增生、不典型增生差异无统计学意义(p = 0.204、p = 0.244、p = 0.204)。免疫组化结果显示,两组间p53、Ki67、Bcl-2的表达差异无统计学意义(p = 0.588、p = 0.662、p = 0.686)。各组间p16表达差异有统计学意义(p = 0.006)。在我们的研究中,链脲佐菌素诱导的实验性糖尿病诱导了p16的表达,但p53、Bcl-2和Ki67的表达没有任何差异。研究中应考虑到DM与口腔癌关系早期的病理改变可能与p16的表达有关;然而,它也可能与p16相关的衰老过程有关。
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The Impact of Type II Diabetes on Tongue Dysplasia and p16-Related Aging Process: An Experimental Study
Objective To evaluate the effect of streptozotocin-induced experimental diabetes mellitus on p16, p53, Ki67, and Bcl2 expressions and histopathological changes in the tongue of the rats. Material and Methods Twenty-two adult female Sprague-Dawley rats were used. The rats were randomly divided into 2 groups (n = 14) as control (C) (n = 8) and diabetic (DM) (n = 6). The rats in the DM group were given streptozotocin as a single intraperitoneal dose for induction of diabetes. Histopathological and immunohistochemical evaluations of formalin-fixed and paraffin-embedded tissue sections of the tongue were used. Results Significant differences were observed between the DM group and the control group in terms of epithelial thickness, length of filiform papillae, and width of filiform papillae (p = 0.005, p = 0.001, and p = 0.006, respectively). There was no significant difference between the groups in terms of mononuclear inflammatory cell infiltration, capillary proliferation, and dysplasia (p = 0.204, p = 0.244, and p = 0.204, respectively). As a result of immunohistochemical studies, no significant difference was found between the groups in terms of p53, Ki67, and Bcl-2 expressions (p = 0.588, p = 0.662, and p = 0.686, respectively). A significant difference was found between the groups when p16 expression was evaluated (p = 0.006). Conclusions In our study, streptozotocin-induced experimental diabetes mellitus induced p16 expression but did not show any difference in p53, Bcl-2, and Ki67 levels. It should be considered in the studies that the pathological changes at the early stages of the relationship between DM and oral cancer may be related to p16 expression; however, it may also be linked with p16-related aging process.
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