玉郎伞多糖对放射性腮腺损伤模型大鼠的保护作用及其机制研究  

Protective Effect and Its Mechanism of Yulangsan Polysaccharide on Rats with Radiation-Induced Parotid Injury

作　　者：李遇春 高艺榕 蒋璐慧 吴兴春 王仁生[2] 黄仁彬[1] Li Yuchun;Gao Yirong;Jiang Luhui;Wu Xingchun;Wang Rensheng;Huang Renbin(College of Pharmacy,Guangxi Medical University,Nanning 530021;The First Affiliated Hospital of Guangxi Medical University,Nanning 530021)

机构地区：[1]广西医科大学药学院,南宁530021 [2]广西医科大学第一附属医院,南宁530021

出　　处：《中药药理与临床》2019年第4期78-84,共7页Pharmacology and Clinics of Chinese Materia Medica

基　　金：国家自然科学基金地区科学基金项目(81560587);广西科学研究与技术开发计划项目(1599005-2-11)

摘　　要：目的:探究玉郎伞多糖对放射性腮腺损伤模型大鼠的保护作用及其机制。方法:将75只雄性SD大鼠随机分为5组,每组15只:正常对照组、模型对照组、玉郎伞多糖150、300、600 mg/kg组。于照射前开始1周各组分别灌胃给予相应药物或生理盐水,连续80日。造模大鼠麻醉后用15 Gy,DTγ射线照射大鼠双侧腮腺组织,正常对照组仅麻醉不予照射。照射后观察大鼠体重,饮食进水等一般情况的改变,分别于照射后第10 d、第40 d、第70 d腹主动脉取血处死大鼠后检测大鼠血清淀粉酶(AMS)及活性氧族(ROS)的含量,肉眼观察大鼠腮腺大体标本后将腮腺完整取下,称取大鼠腮腺质量,取部分腮腺进行HE染色、TUNEL染色及免疫组织化学法检测B淋巴细胞瘤-2基因(Bcl-2)、Bcl2-Associated X的蛋白质(Bax)、增殖细胞核抗原(PCNA)及肿瘤坏死因子(TNF-α)的表达。结果:与正常组比较,模型组血清AMS含量,先明显升高后显著降低,血清ROS含量明显升高,细胞凋亡率明显升高,腮腺组织中Bcl-2表达明显下调,Bax、PCNA、TNF-α蛋白表达明显上调。玉郎伞多糖可改善照射后大鼠腮腺的损伤,减少腮腺细胞的凋亡率及下调Bax、PCNA、TNF-α蛋白的阳性表达率,上调Bcl-2蛋白的阳性表达率,明显降低血清中ROS含量,先降低后增高血清AMS含量。结论:玉郎伞多糖对放射性腮腺损伤模型大鼠有保护作用,其机制可能与抑制腮腺细胞凋亡及清除大鼠照射后ROS活性有关。Objective: To explore the protective effect and its mechanism of Yulangsan polysaccharides (YLSP) on rats with radiation-induced parotid injury. Methods: 75 SD rats were randomly divided into 5 groups: the control group,the model group,150,300 and 600 mg/kg Yulangsan polysaccharides (YLSP) groups. Corresponding drugs or saline water were administered from one week before irradiation,for 80 days. Except for the control group,all rats were irradiated with 15 Gy/times γ-rays on parotid to establish the model. After the irradiation,the changes of general conditions such as body weight,dietary water intake were observed. Rats were sacrificed on the 10 th,40 th,and 70 th days after irradiation by taking blood from the abdominal aorta,then amylase (AMS) and reactive oxygen species (ROS) levels were detected. Parotid gland tissues were collected and weighed. Expressions of B-cell lymphoma-2,Bcl2-Associated X,proliferating cell nuclear antigen and Tumor necrosis factor-αin parotid gland were determined by HE staining,TUNEL staining and immunohistochemistry. Results:Compared with the control group,the serum AMS content in the model group was firstly increased but then decreased significantly,the serum level of ROS and apoptosis rate were increased. The expression of Bcl-2 was down regulated and expressions of Bax,PCNA and TNF-α protein were up regulated. Compared with the model group,YLSP improved the pathological changes of parotid gland after radiation and reduced the apoptosis rate of parotid cells,it decreased the positive expression rates of Bax,PCNA and TNF-α protein,and up regulated the positive expression rate of Bcl-2 protein,it also reduced the level of ROS,and significantly increased serum AMS content after decreased AMS firstly.Conclusion: YLSP can protect against radiation-induced parotid injury in rats. The mechanism may be related to inhibiting the apoptosis of parotid gland cells and reducing ROS.

关 键 词：玉郎伞多糖 放射性腮腺损伤 凋亡因子 ROS TNF-Α 

分 类 号：R73[医药卫生—肿瘤]