芹菜素对呕吐毒素引起KM小鼠肠道损伤的保护作用OA
Protective Effects of Apigenin against Deoxynivalenol-induced Intestinal Injury in KM Mice
基于呕吐毒素(DON)引起的KM小鼠肠道损伤,为了探讨芹菜素(API)的保护作用并揭示其潜在机制,将健康雄性KM小鼠随机分为空白组、DON组、低剂量API组、高剂量API组、低剂量API干预组(低剂量API+DON)和高剂量API干预组(高剂量API+DON).通过小鼠体质量监测、结肠组织苏木精-伊红病理染色、TUNEL凋亡染色、Western blotting凋亡相关蛋白表达检测、血清乳酸脱氢酶(LDH)、总超氧化物歧化酶(SOD)、丙二醛(MDA)含量测定等,综合评估芹菜素对呕吐毒素引起KM小鼠肠道损伤的保护作用.研究结果表明,与空白组相比,DON组小鼠体质量在第19天达到峰值后显著下降,经高剂量API干预后小鼠体质量下降趋势得到缓解.病理检测发现高剂量API干预后结肠组织损伤得到改善,与DON组相比损伤病理评分降低1.3.TUNEL染色显示API干预后显著降低凋亡细胞数量,Western blotting进一步证实API干预下调了凋亡蛋白Bax、P53、Caspase-12和Caspase-9的表达并降低了 Bcl-2的表达.血清学检测发现,与DON组相比,高剂量API干预将LDH水平降低了 7.53%(P<0.05),SOD活性提高了 46.82%(P<0.05),MDA含量降低了 12.25%(P<0.05).因此,上述结果表明API对DON引起的KM小鼠肠道损伤具有显著的保护作用,其作用机制可能与抑制DON引起的结肠组织细胞凋亡以及改善小鼠血清LDH和SOD酶活性等多途径协同作用相关.本研究为API作为功能性食品成分在预防和治疗DON相关肠道损伤中的潜在应用提供了有力的理论支持.
Based on the intestinal damage induced by deoxynivalenol(DON)in KM mice,to investigate the protective effect of apigenin(API)and reveal its potential mechanism,healthy male KM mice were randomly divided into a control group,a DON group,a low-dose API group,a high-dose API group,a low-dose API intervention group(low-dose API+DON),and a high-dose API intervention group(high-dose API+DON).The protective effects of API against DON-induced intestinal injury in KM mice were comprehensively assessed through multiple approaches:monitoring of body weight,pathological staining of colonic tissue with hematoxylin-eosin,TUNEL apoptosis staining,western blotting analysis of apoptosis-related protein expression,and measurement of serum lactate dehydrogenase(LDH),total superoxide dismutase(SOD),and malondialdehyde(MDA)levels.The results showed that,compared with the blank group,the DON group exhibited significantly decreased body weight after peaking on day 19,and high-dose API intervention successfully mitigated the trend of weight loss.Pathological examination revealed that colonic tissue damage improved after high-dose API intervention,and the pathological score of damage was reduced by 1.3 when compared with that of the DON group.TUNEL staining showed that API interventions significantly reduced the count of apoptotic cells.Western blot analysis further confirmed that API intervention downregulated the expression of apoptotic proteins Bax,P53,caspase-12,and caspase-9 and decreased the expression of Bcl-2.Serological assays revealed that,compared with the DON group,high-dose API intervention reduced LDH level by 7.53%(P<0.05),increased SOD activity by 46.82%(P<0.05),and reduced MDA level by 12.25%(P<0.05).These results indicate that API has a significant protective effect on DON-induced intestinal injury in KM mice,and the mechanism may be related to the synergistic effects of multiple pathways,including the inhibition of DON-induced apoptosis in colonic tissue as well as improvement of serum LDH and SOD activities in the mice.This study provides strong theoretical support for the potential application of API as a functional food ingredient in the prevention and treatment of DON-related intestinal injury.
李苏冰;张百刚;焦禄;黄橙辉;徐冬梅;石文贵
兰州理工大学生命科学与工程学院,甘肃兰州 730050兰州理工大学生命科学与工程学院,甘肃兰州 730050兰州理工大学生命科学与工程学院,甘肃兰州 730050兰州理工大学生命科学与工程学院,甘肃兰州 730050兰州理工大学生命科学与工程学院,甘肃兰州 730050兰州大学第二医院临床医学院萃英生物医学研究中心,甘肃兰州 730000
芹菜素呕吐毒素肠道损伤抗氧化细胞凋亡
apigenindeoxynivalenolintestinal injuryantioxidantcell apoptosis
《现代食品科技》 2026 (4)
32-39,8
甘肃省高等学校科研项目(2016B-024)甘肃省自然科学基金项目(18JR3RA136)国家自然科学基金地区科学基金项目(31760495)中央高校基本科研经费资助(lzujbky-2024-ey05)甘肃省科技计划项目(G1906)国家自然基金地区项目(31960491)
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