Effects of Codonopsis pilosula polysaccharide on gastric mucosal injury in rats with chronic atrophic gastritis
OBJECTIVE To investigate the effects of Codonopsis pilosula polysaccharide(CPP)regulating the nuclear factor-erythroid 2-related factor 2(Nrf2)/heme oxygenase-1(HO-1)signaling pathway on gastric mucosal injury in rats with chronic atrophic gastritis(CAG).METHODS Rats were randomly divided into control group,model group,CPP low-dose,medium-dose and high-dose groups(CPP 10,20,40 mg/kg),and ML385 group(Nrf2 inhibitor ML385 30 mg/kg+CPP 40 mg/kg),10 rats per group.CAG rat model was established using N-methyl-N′-nitro-N-nitrosoguanidine combined with irregular diet,then they were given drugs for consecutive 6 weeks.HE staining was used to observe the pathological changes in gastric tissue morphology;the levels of serum gastrin(GAS),motilin(MTL),pepsin(PP),as well as tumor necrosis factor-α(TNF-α),interleukin-8(IL-8)malondialdehyde(MDA)and superoxide dismutase(SOD)in gastric mucosal tissue were detected;TUNEL assay was used to observe gastric mucosal tissue cell apoptosis;immunohistochemical assay was adopted to observe the expressions of Nrf2 and recombinant Bcl2 associated X protein(Bax)in gastric mucosal tissue;Western blot was used to detect the expressions of Nrf2,HO-1,Bax and Bcl-2 proteins in gastric mucosal tissue.RESULTS Compared with the control group,the gastric mucosal tissue was damaged;the levels of GAS,MTL,PP and SOD,and the protein expressions of Nrf2,HO-1 and Bcl-2 were significantly reduced in model group(P＜0.05),while the levels of MDA,TNF-α and IL-8,the cell apoptosis index,and the protein expression of Bax were significantly increased(P＜0.05).Compared with model group,CPP low-dose,medium-dose and high-dose groups showed varying degrees of improvement in gastric mucosal histopathology;the levels of the quantitative indicators were significantly reversed(P＜0.05).Nrf2 inhibitor ML385 significantly attenuated the improvement effect of high-dose CPP on the above indicators in CAG rats(P＜0.05).CONCLUSIONS CPP can improve gastric mucosal injury in CAG rats,and inhibit oxidative stress,inflammatory response,and cell apoptosis.The mechanism of action may be related to the activation of Nrf2/HO-1 signaling pathway.
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