红景天苷通过VIP-cAMP通路对大鼠腮腺放射性损伤的改善作用及机制
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| 篇名: | 红景天苷通过VIP-cAMP通路对大鼠腮腺放射性损伤的改善作用及机制 |
| TITLE: | Improvement effect and mechanism of salidroside on radiation-induced parotid gland injury in rats by VIP-cAMP pathway |
| 摘要: | 目的 探讨红景天苷对大鼠腮腺放射性损伤的改善作用及机制。方法将大鼠随机分为正常组、放射组、红景天苷低剂量(红景天苷-L,50mg/kg)组、红景天苷高剂量(红景天苷-H,100mg/kg)组、红景天苷-H+抑制剂(100mg/kg红景天苷+0.1µmol/kgH-89)组,每组10只。除正常组外,其余各组大鼠通过放射线照射构建腮腺放射性损伤模型。各组大鼠腹腔注射相应药物或生理盐水,每日1次,连续40d。末次给药后,检测血清中活性氧(ROS)、环磷酸腺苷(cAMP)、超氧化物歧化酶(SOD)、淀粉酶水平,观察腮腺组织病理学变化,检测腮腺组织细胞凋亡率和其中B细胞淋巴瘤2(Bcl-2)及其相关X蛋白(Bax)表达情况,白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)mRNA表达水平,以及Ⅲ型胶原蛋白(ColⅢ)、血管活性肠肽(VIP)蛋白表达水平和cAMP依赖性蛋白激酶(PKA)磷酸化水平。结果与正常组比较,放射组大鼠ROS、淀粉酶水平,细胞凋亡率、Bax表达水平和IL-6、TNF-αmRNA表达水平以及ColⅢ蛋白表达水平均显著升高,cAMP、SOD水平,Bcl-2表达水平和VIP蛋白表达水平及PKA磷酸化水平均显著降低(P<0.05);与放射组比较,红景天苷-L组和红景天苷-H组大鼠上述指标均显著改善(P<0.05),且红景天苷-H组改善更明显(P<0.05);抑制剂H-89显著逆转了红景天苷-H组大鼠上述指标的变化(P<0.05)。结论红景天苷可有效改善大鼠的腮腺放射性损伤,其机制可能与激活VIP-cAMP通路有关。 |
| ABSTRACT: | OBJECTIVE To explore the improvement effect and mechanism of salidroside on radiation-induced parotid gland injury in rats. METHODS Rats were randomly assigned into normal group, radiation group, salidroside low-dose (salidroside-L, 50 mg/kg) group, salidroside high-dose (salidroside-H, 100 mg/kg) group, and salidroside-H+inhibitor (100 mg/kg salidroside+0.1 µmol/kg H-89) group, with 10 rats in each group. Except for the normal group, rats in the other groups were subjected to radiation exposure to establish a model of radiation-induced parotid gland injury. Rats in each group were intraperitoneally injected with the corresponding drug or normal saline, once a day, for 40 consecutive days. After the last administration, the levels of reactive oxygen species (ROS), cyclic adenosine monophosphate (cAMP), superoxide dismutase (SOD), and amylase in serum were detected; the pathological changes of parotid gland tissue were observed; the apoptosis rate of parotid gland tissue cells, the expression levels of B-cell lymphoma-2 (Bcl-2) and its associated X protein (Bax), mRNA expression levels of interleukin-6 (IL- 6) and tumor necrosis factor-α (TNF-α), the protein expression levels of type Ⅲ collagen (Col Ⅲ), vasoactive intestinal peptide (VIP), and the phosphorylation level of protein kinase A (PKA) in parotid gland tissue were determined. RESULTS Compared with normal group, the levels of ROS, amylase, apoptosis rate, Bax expression level, mRNA expression levels of IL-6 and TNF- α, and protein expression level of Col Ⅲ in the radiation group were significantly increased, while the levels of cAMP, SOD, Bcl-2 expression level, VIP protein expression level and PKA phosphorylation level were significantly decreased (P<0.05). Compared with radiation group, the above indicators in the salidroside-L group and salidroside-H group were significantly improved (P<0.05), and the improvement in the salidroside-H group was more significant (P<0.05); inhibitor H-89 significantly reversed the changes in the above indicators of the salidroside-H group (P<0.05). CONCLUSIONS Salidroside can effectively alleviate radiation-induced parotid gland injury in rats, and its mechanism may be related to the activation of the VIP-cAMP pathway. |
| 期刊: | 2025年第36卷第22期 |
| 作者: | 张春英;阴广维;陈红;尤鸣达;刘金凤;张亚昆;胡耀杰 |
| AUTHORS: | ZHANG Chunying,YIN Guangwei,CHEN Hong,YOU Mingda,LIU Jinfeng,ZHANG Yakun,HU Yaojie |
| 关键字: | 红景天苷;放射性损伤;腮腺;VIP-cAMP通路 |
| KEYWORDS: | salidroside; radiation injury; parotid gland; VIP-cAMP pathway |
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