Improvement effect and mechanism of salidroside on radiation-induced parotid gland injury in rats by VIP-cAMP pathway
- VernacularTitle: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
- Author:
Chunying ZHANG
1
;
Guangwei YIN
2
;
Hong CHEN
1
;
Mingda YOU
1
;
Jinfeng LIU
3
;
Yakun ZHANG
2
;
Yaojie HU
1
Author Information
1. Dept. of Head and Neck Surgery，Tangshan Workers’Hospital，Hebei Tangshan 063000，China
2. Dept. of Surgery，Tangshan Workers’Hospital，Hebei Tangshan 063000，China
3. Dept. of Surgery，the Affiliated Hospital of North China University of Science and Technology，Hebei Tangshan 063000，China
- Publication Type:Journal Article
- Keywords:
salidroside;
radiation injury;
parotid gland;
VIP-cAMP pathway
- From:
China Pharmacy
2025;36(22):2796-2801
- CountryChina
- Language:Chinese
-
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.
