机构地区:[1]山西农业大学食品科学与工程学院,山西晋中030801 [2]山西省食用菌工程技术研究中心,山西晋中030801 [3]黄土高原食用菌山西省重点实验室,山西晋中030801
出 处:《食用菌学报》2025年第2期39-48,共10页Acta Edulis Fungi
基 金:山西省基础研究计划青年项目(20210302124071);食用菌山西省科技创新重点团队(201805D131009)。
摘 要:通过对小鼠连续3 d腹腔注射环磷酰胺(cyclophosphamide, CY),构建小鼠肝脏损伤模型,灌胃鳞杯伞(Clitocybe squamulosa)多糖(C. squamulosa fruiting body polysaccharide,CSFP)溶液(200、400、800mg·kg^(-1));测定小鼠肝脏组织中超氧化物歧化酶(superoxide dismutase, SOD)、过氧化氢酶(catalase,CAT)、谷胱甘肽过氧化物酶(glutathioneperoxidase,GSH-Px)、丙二醛(malondialdehyde,MDA)和谷胱甘肽(glutathione, GSH)的含量;测定肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)、白细胞介素-1β(interleukin-1β, IL-1β)、白细胞介素-6(interleukin-6, IL-6)、白细胞介素-10(interleukin-10, IL-10)的含量;检测SOD、CAT、核因子E2相关因子(nuclear factor erythroid-2 related factor 2, Nrf2)、血红素加氧酶-1(heme oxygenase-1,HO-1)、环氧合酶-2(cyclooxygenase-2,COX-2)、诱导型一氧化氮合酶(induciblenitricoxide synthase,iNOS)的mRNA相对表达水平。结果表明:与模型组(CY组)相比,鳞杯伞多糖组小鼠体质量增加,进食、饮水情况均有所改善;鳞杯伞多糖组小鼠肝脏SOD、CAT、GSH-Px活力显著升高,MDA水平下降,GSH水平显著提升;与模型组(CY组)相比,鳞杯伞多糖组TNF-α、IL-1β和IL-6的含量显著降低,IL-10的含量显著上升;荧光定量PCR显示,CSFP能显著抑制CY处理小鼠的Nrf2和HO-1异常下降以及iNOS和COX-2的表达异常上升。CSFP能抑制CY诱导的肝脏脂质过氧化;改善炎性细胞因子的分泌水平;激活Nrf2/HO-1信号通路改善氧化应激;抑制炎症反应相关因子iNOS、COX-2的mRNA相对表达水平,研究结果表明CSFP可能通过干预氧化应激和炎症反应等途径,发挥对CY引起的肝脏损伤的保护作用。Mice were intraperitoneally injected with cyclophosphamide(CY) for three consecutive days to establish a liver injury model. Then, Clitocybe squamulosa fruiting body polysaccharide(CSFP) solution was administered to the model mice at 200, 400 and 800 mg·kg^(-1) by gavage, respectively. Different dose groups were then determined for contents of superoxide dismutase(SOD), catalase(CAT), glutathione peroxidase(GSHPx), malondialdehyde(MDA), glutathione(GSH), tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β),interleukin-6(IL-6) and interleukin-10(IL-10) in liver tissue. The mRNA levels of SOD, CAT, nuclear factor E2 related factor 2(Nrf2), heme oxygenase-1(HO-1), cyclooxygenase-2(COX-2) and inducible nitric oxide synthase(iNOS) were also determined. The results showed that compared with the model group(CY), the CSFP groups showed increases in body weight, water intake and food intake. The activities of SOD, CAT and GSHPx in the CSFP groups were significantly increased, and their MDA and GSH levels were significantly decreased and increased, respectively. Compared with the model group, the contents of TNF-α、IL-1β and IL-6 in the CSFP groups decreased significantly, whereas the content of IL-10 in all CSFP groups increased significantly.Fluorescence quantitative PCR showed that CSFP significantly inhibited abnormal decreases in Nrf2 and HO-1expression, and abnormal increases in iNOS and COX-2 expression in the model group. In summary, CSFP inhibited the hepatic lipid peroxidation induced by CY, improved the secretion of inflammatory cytokines,activated the Nrf2/HO-1 signaling pathway to alleviate oxidative stress, and inhibited the mRNA expression of iNOS and COX-2. These results suggested that CSFP may exert its protective effect on cyclophosphamideinduced liver injury through intervening oxidative stress and inflammatory reactions.
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