研究报告

植物乳杆菌HFY09通过调控TGF-β1表达对小鼠狼疮性肾炎的干预作用

  • 易若琨 ,
  • 赵欣 ,
  • 刘佳 ,
  • 杨贞耐
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  • 1(北京工商大学老年营养与健康教育部重点实验室,北京,100048)
    2(儿童营养与健康发展创新中心(重庆第二师范学院),重庆,400067)
博士研究生(杨贞耐教授为通信作者,E-mail:yangzhennai@th.btbu.edu.cn)

收稿日期: 2022-07-26

  修回日期: 2022-09-10

  网络出版日期: 2023-06-05

基金资助

重庆市高校创新研究群体项目(CXQTP20033)

Intervention effect of Lactobacillus plantarum HFY09 on lupus nephritis in mice by regulating TGF-β1 expression

  • YI Ruokun ,
  • ZHAO Xin ,
  • LIU Jia ,
  • YANG Zhennai
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  • 1(Key Laboratory of Geriatric Nutrition and Health of Ministry of Education, Beijing Technology and Business University, Beijing 100048, China)
    2(Collaborative Innovation Center for Child Nutrition and Health Development, Chongqing University ofEducation, Chongqing 400067, China)

Received date: 2022-07-26

  Revised date: 2022-09-10

  Online published: 2023-06-05

摘要

该研究观察了一株分离于自然发酵牦牛酸乳的植物乳杆菌HFY09(Lactobacillus plantarum HFY09,LP-HFY09),通过降植烷建立狼疮性肾炎动物模型验证了LP-HFY09的作用,并通过试剂盒法、苏木精-伊红染色法、qPCR和Western blot检测小鼠血清和肾组织的相关指标。实验结果显示,LP-HFY09能够降低狼疮性肾炎造成的尿蛋白升高和血清、肾组织白介素6(interleukin-6,IL-6)、IL-12、TNF-α和IFN-γ细胞因子水平升高。LP-HFY09还可以降低肾炎小鼠血清肌酐、尿素氮、总胆固醇、甘油三酯水平和提高总蛋白、白蛋白水平。另外LP-HFY09具有抑制肾炎小鼠抗双链DNA抗体阳性率的作用。切片观察发现LP-HFY09能够减轻肾炎造成的肾小球形态不完整和炎性浸润等组织损伤。LP-HFY09还能够下调狼疮性肾炎小鼠肾脏组织中的转化生长因子-β1(transforming growth factor-β1,TGF-β1)和血管内皮生长因子mRNA和蛋白表达和上调铜锌超氧化物歧化酶和锰超氧化物歧化酶表达。结果表明,LP-HFY09能够对狼疮性肾炎起到明显的干预作用,且LP-HFY09的作用与其浓度呈正相关,在109 CFU/kg作用下效果接近药物泼尼松。

本文引用格式

易若琨 , 赵欣 , 刘佳 , 杨贞耐 . 植物乳杆菌HFY09通过调控TGF-β1表达对小鼠狼疮性肾炎的干预作用[J]. 食品与发酵工业, 2023 , 49(9) : 32 -39 . DOI: 10.13995/j.cnki.11-1802/ts.033107

Abstract

In this study, a strain of Lactobacillus plantarum HFY09 (LP-HFY09) isolated from naturally fermented yak yoghurt was observed, and an animal model of lupus nephritis was established using pristane to verify the effect of LP-HFY09. The related indexes of mouse serum and kidney tissue were detected by kit method, hematoxylin-eosin staining (H&E) method, quantitative polymerase chain reaction (qPCR) and Western blot. The experimental results showed that LP-HFY09 could reduce the increase of urinary protein and the increase of serum and renal tissue interleukin-6 (IL-6), IL-12, tumor necrosis factor alpha (TNF-α), interferon γ (IFN-γ) cytokine levels caused by lupus nephritis. LP-HFY09 could also reduce serum creatinine (SCr), blood urea nitrogen (BUN), total cholesterol (TC), triglyceride (TG) levels and increase total protein (TP), albumin (ALB) levels in nephritis mice. In addition, LP-HFY09 could inhibit the positive rate of anti-double-stranded deoxyribonucleic acid (dsDNA) in mice with nephritis. Section observation showed that LP-HFY09 could reduce tissue damage such as incomplete glomerular morphology and inflammatory infiltration caused by nephritis. LP-HFY09 can also down-regulate mRNA and protein expressions of transforming growth factor-β1 (TGF-β1), vascular endothelial growth factor (VEGF) and Cu/Zn-SOD, Mn-SOD expressions in the kidney tissue of lupus nephritis mice. These results indicated that LP-HFY09 could play a significant role in interfering with lupus nephritis, and the effect of LP-HFY09 was positively correlated with its concentration, and its effect was close to that of the drug prednisone under the action of 109 CFU/kg.

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