发酵粘液乳杆菌CQPC08调节氧化应激和运动能力的效果

陆文娟; 宋灿琳; 赵茹兰; 赵欣

doi:10.13386/j.issn1002-0306.2026050083

发酵粘液乳杆菌CQPC08调节氧化应激和运动能力的效果

Effect of Limosilactobacillus fermentum CQPC08 on Regulating Oxidative Stress and Exercise Capacity

摘要

摘要: 本研究通过D-半乳糖诱导构建小鼠氧化应激模型，探讨发酵粘液乳杆菌CQPC08（Limosilactobacillus fermentum CQPC08，LF-CQPC08）对肝脏氧化应激状态及运动耐力的影响。实验通过力竭跑步测试评估小鼠运动能力，采用试剂盒检测血清与肝组织相关指标，并借助苏木精-伊红（H&E）染色观察肝组织病理形态。此外，运用定量聚合酶链反应技术（quantitative polymerase chain reaction，qPCR）对肝组织、腓肠肌组织及肠道内容物中特定基因的mRNA表达进行测定。结果表明，与模型组相比，LF-CQPC08干预显著延长了小鼠力竭跑步时间（49.5±5.3 min）；降低血清中乳酸（lactic acid，LA，4.99±0.28 mmol/L）、肌酸激酶（creatine kinase，CK，336.79±35.05 U/L）及脂多糖（lipopolysaccharide，LPS，0.18±0.02 pg/mL）含量；提高肝糖原（hepatic glycogen，HG，10.87±1.57 mg/g）与肌糖原（muscle glycogen，MG，1.65±0.20 mg/g）储备，同时降低肿瘤坏死因子-α（tumor necrosis factor-alpha，TNF-α，74.56±8.62 pg/mg）、白细胞介素-6（interleukin-6，IL-6，80.14±7.71 pg/mg）及活性氧（reactive oxygen species，ROS，4.54±0.22×10³ RFU荧光强度）水平。肝组织切片显示，LF-CQPC08减轻了氧化应激引起的病理损伤。进一步的分子检测发现，LF-CQPC08能上调氧化应激力竭小鼠肝组织与腓肠肌中超氧化物歧化酶1（superoxide dismutase 1，SOD1）、SOD2、过氧化氢酶（catalase，CAT）及谷胱甘肽过氧化物酶4（glutathione peroxidase 4，GPx4）的mRNA表达。同时，LF-CQPC08还能够上调氧化损伤小鼠腓肠肌组织的SOD2和CAT蛋白表达。肠道内容物分析显示，LF-CQPC08可增加模型小鼠双歧杆菌、乳杆菌、直肠真杆菌、柔嫩梭菌、梭菌的相对丰度和降低肠球菌、脱硫弧杆菌相对丰度，特别是能够显著提升乳杆菌的相对丰度，其水平甚至超过正常组。以上结果提示，LF-CQPC08具有缓解氧化损伤及增强运动耐力的作用。

Abstract: In this study, a mouse model of oxidative stress was established by D-galactose induction to investigate the effects of Limosilactobacillus fermentum CQPC08(LF-CQPC08) on hepatic oxidative stress and exercise endurance. The exercise capacity of mice was evaluated using an exhaustive running test. Relevant biomarkers in serum and liver tissue were measured using assay kits, and hepatic histopathology was observed via hematoxylin and eosin(H&E) staining. Additionally, quantitative polymerase chain reaction(qPCR) was employed to determine the mRNA expression levels of specific genes in the liver tissue, gastrocnemius muscle tissue, and intestinal contents. The results indicated that, compared with the model group, LF-CQPC08 intervention significantly prolonged the exhaustive running time (49.5±5.3 min) of mice. It reduced serum levels of lactic acid(LA, 4.99±0.28 mmol/L), creatine kinase(CK, 336.79±35.05 U/L), and lipopolysaccharide(LPS, 0.18±0.02 pg/mL), while increasing the reserves of hepatic glycogen(HG, 10.87±1.57 mg/g) and muscle glycogen(MG, 1.65±0.20 mg/g). Furthermore, it decreased the levels of tumor necrosis factor-alpha(TNF-α, 74.56±8.62 pg/mg), interleukin-6(IL-6, 80.14±7.71 pg/mg), and reactive oxygen species(ROS, 4.54±0.22×10³ RFU fluorescence intensity). Histopathological examination of liver sections revealed that LF-CQPC08 alleviated oxidative stress-induced tissue damage. Further molecular analyses demonstrated that LF-CQPC08 up-regulated the mRNA expression of superoxide dismutase 1(SOD1), SOD2, catalase(CAT), and glutathione peroxidase 4(GPx4) in the liver and gastrocnemius muscle of mice subjected to exhaustive exercise under oxidative stress. Additionally, LF-CQPC08 also upregulated the protein expression of SOD2 and CAT in the gastrocnemius tissue of oxidatively damaged mice. Analysis of intestinal contents showed that LF-CQPC08 increased the relative abundance of Bifidobacterium, Lactobacillus, Eubacterium rectale, Faecalibacterium prausnitzii, and Clostridium in model mice, while decreasing the relative abundance of Enterococcus and Desulfovibrio. Notably, it significantly elevated the relative abundance of Lactobacillus to a level even higher than that in the normal group. These findings suggest that LF-CQPC08 possesses the potential to mitigate oxidative damage and improve physical endurance.