| Summary: | Objective To study the protective effect of Lycium barbarum polysaccharide (LBP) against apoptosis of small intestinal epithelial cells (IECs) in mice with radiation-induced intestinal injury and explore the pathway that mediates this effect. Methods A mouse model of radiation-induced intestinal injury was established using a linear accelerator. In 2 h after the radiation exposure, the mice were treated with 200, 400, or 800 mg/kg LBP by gavage for 7 d (LBP intervention groups) or with normal saline (radiation group), and the mice without any treatment and those treated with 800 mg/kg LBP by gavage without X-ray radiation served as the control groups. After the treatments, the intestinal segment near the duodenum was dissected for pathological examination. The viability of the IECs isolated from the intestines of the mice was evaluated with CCK-8 assay, the cell apoptosis rate was detected with flow cytometry, and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were determined by spectrophotometry; Western blotting was performed to detect the expression levels of apoptosis regulators Bcl-2 and Bax in the IECs. Results Compared with the mice in the radiation group, those in LBP intervention groups showed greater intestinal villus length and crypt number and higher viability of the IECs at 7 d after the radiation (P < 0.05). The increase of LBP concentration significantly increased SOD activity (1.22±0.05 U/mL at 200 mg/kg, 1.32±0.06 U/mL at 400 mg/kg, and 1.53±0.03 U/mL at 800 mg/kg) and lowered the apoptotic rate and MDA content in the IECs. Compared with the IECs in the radiation group, the cells from LBP intervention groups showed significantly increased expression of Bcl-2 (nearly doubled at the LBP dose of 800 mg/kg) and lowered expression of Bax (by about 50% at the LBP dose of 800 mg/kg). Conclusion For mice with radiation-induced intestinal injury, LBP treatment suppresses apoptosis of IECs by regulating Bcl-2 and Bax expressions and enhances their antioxidant capacity by increasing SOD activity and decreasing the content of MDA.
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