The therapeutic effect of Balanophora polysaccharide on acetic acid gastric ulcer in rats and its mechanism
- Author:
De-Yao XIA
1
;
Fang-Yu ZHAO
1
;
Xian-Bing CHEN
1
;
De-Yao XIA
2
;
Sheng-Zhe HUANG
2
;
Yi-Ru ZHAO
2
;
Jiang-Hua WANG
2
;
Jun-Yan MOU
2
;
Feng-Jie WANG
2
;
Xian-Bing CHEN
2
Author Information
- Publication Type:Journal Article
- Keywords: Balanophora polysaccharide; epidermal growth factor; epidermal growth factor receptor; gastric ulcer; inflammation; oxidative stress
- From: Chinese Pharmacological Bulletin 2023;39(1):193-199
- CountryChina
- Language:Chinese
- Abstract: Aim To study the therapeutic effect of Balanophora polysaccharide(BPS)on gastric ulcer(GU)induced by acetic acid in rats and to investigateits mechanisms. Methods Sixty male SD rats were randomly divided into sham-operated group, GU model group, omeprazole positive group(3.6 mg·kg-1), and low, medium and high dose of BPS treatment groups(100, 200 and 400 mg·kg-1). The GU model group was prepared by acetic acid cautery method, and the morphology and pathological changes of ulcers were observed by visual observation combined with HE staining, and the ulcer area and inhibition rate were measured and calculated; superoxide dismutase(SOD)activity, malondialdehyde(MDA)content and glutathione peroxidase(GSH-PX)activity were measured by enzymatic assay; tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)content were detected by ELISA. The expression levels of epidermal growth factor(EGF)and epidermal growth factor receptor(EGFR)were measured by immunohistochemistry staining and Western blot. Results Compared with the sham-operated group, obvious ulcer damage was seen in the model group. Compared with the model group, the BPS-treated group showed a significant reduction in ulcer area, an increase in SOD and GSH-PX activity and EGF and EGFR expression levels, and a significant decrease in MDA, TNF-α and IL-6 content. Conclusions BPS has a therapeutic effect on GU in rats, and its mechanism may be related to the inhibition of oxidative stress, suppression of inflammatory stimuli and promotion of regenerative repair of gastric mucosa.
