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作 者:敖翔[1] 王丽娜[1] 王娇娇[1] 叶丹丹[1] 丁印浩 曲文姝 牛卫东[1]
机构地区:[1]大连医科大学口腔医学院口腔内科教研室,辽宁大连116044
出 处:《口腔医学研究》2017年第1期1-5,共5页Journal of Oral Science Research
基 金:国家自然科学基金(编号:81171538)
摘 要:目的:检测大鼠根尖周炎中Jak2-Stat3信号通路的表达。方法:将25只8周龄SD大鼠右下颌第一磨牙开髓,封入PBS缓冲液小棉球,进口玻璃离子暂封,调合。分别于术后0、7、14、21、28d处死后取下颌骨组织,制备石蜡切片后,采用HE染色检测根尖周炎症进展过程,免疫组织化学的方法检测Jak2、P-Jak2、Stat3、P-Stat3的表达。酶组织化学方法检测破骨细胞的表达。结果:成功建立了PBS感染的大鼠根尖周炎模型。Jak2、Stat3、PJak2和P-Stat3在正常组织中少量表达。炎症进展至14d,Jak2、P-Jak2、Stat3、P-Stat3表达均达到顶峰,明显高于对照组(P<0.05);21d时,Jak2、P-Jak2、Stat3、P-Stat3数量有一定减少,但仍高于对照组(P<0.05),28d时,Jak2、P-Jak2、Stat3、P-Stat3均明显降低,Stat3、P-Jak2和P-Stat3表达与对照组相似(P>0.05);Jak2稍高于对照组(P<0.05)。破骨细胞在7d表达增多(P<0.05),14d时达到顶峰(P<0.05),21、28d表达下降但仍高于对照组(P<0.05)。结论:Jak2/Stat3信号通路与根尖周炎症的急性期的炎症进展过程密切相关,推测其在根尖周急性炎症期骨破坏过程中发挥了重要作用。Objective:To investigate the expression of Jak2/Stat3 pathway in induced rat inflammatory periapical lesions.Methods:Pulps of right mandibular first molars of twenty-five 8-week-old SD rats were exposed with PBS cotton ball.Then the molars were filled with glass ionomer and occulsal relationship was adjusted.The rats were then randomly sacrificed after 0,7,14,21 and 28days.The lower jaws were isolated and prepared for histologic,immunohistochemical,and enzyme histochemical analysis.Results:The model of apical periodontitis by PBS was successfully induced.The number of Jak2,Stat3,P-Jak2 and P-Stat3 positive cells was higher in periapical lesions compared with normal root apices(P〈0.05),and peaked at 14 days and decreased at 21days(P〈0.05).On 28 days,the expressions of Stat3,P-Jak2 and P-Stat3 in the experimental group were almost the same as those of the control group(P〉0.05).However,the expression of Jak2 was still higher than that in the control group(P〈0.05).The formation of osteoclasts in the experimental group increased after 7days,reached the maximum after 14 days and decreased after 21 and 28days in contrast to that of the control group(P〈0.05).The expression of Jak2/Stat3 was found synchronous with osteoclast formation.Conclusion:These findings suggest that Jak2/Stat3 pathway may play an important role in the periapical periodontitis and contribute to the initiation of periapical bone destruction.
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