细粒棘球蚴抗原B对小鼠脓毒症脑病的保护作用

    Protective effect of Echinococcus granulosus antigen B on sepsis-associated encephalopathy in mice

    • 摘要:
      目的: 观察细粒棘球蚴抗原B(AgB)对细菌脂多糖(LPS)诱导的小鼠脓毒症脑病(SAE)的作用效果。
      方法: 18只雄性C57bl/6小鼠随机分成正常对照组(A组)、SAE模型组(B组)、蛋白干预组(C组),每组6只。A组腹腔注射PBS;B组和C组应用LPS腹腔内注射诱导小鼠SAE,B组腹腔注射PBS,C组腹腔注射含5% AgB的PBS溶液。通过ELISA测定抑炎因子白细胞介素–10(IL–10)、转化生长因子–β(TGF–β)以及促炎因子肿瘤坏死因子–α(TNF–α)和白细胞介素–6(IL–6)的水平。通过全自动生化分析仪检测小鼠肝肾功能指标,包括丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、血清肌酐肌酐(Cr)以及尿素(UREA)的水平。HE染色观察小鼠脑组织脑损伤情况,免疫组织化学染色检测离子钙接头分子1(lba–1)阳性细胞数目情况。
      结果: 与A组相比,B组小鼠脑组织损伤加重,血清促炎因子TNF–α、IL–6水平明显升高,抗炎因子IL–10、TGF–β水平明显降低,ALT、AST、CR及UREA含量明显升高,脑组织lba–1阳性细胞数明显增加(P < 0.01)。与B组相比,C组小鼠脑组织损伤减轻,血清中促炎因子TNF–α、IL–6水平明显降低,抗炎因子IL–10、TGF–β水平明显升高,ALT、AST、CR及UREA含量明显降低,脑组织lba–1阳性细胞数明显减少(P < 0.01)。
      结论: AgB对LPS诱导的SAE小鼠具有保护作用,可能与抑制小胶质细胞活化相关。

       

      Abstract:
      Objective To observe the effect of Echinococcus granulosus antigen B (AgB) on bacterial lipopolysaccharide (LPS)-induced sepsis-associated encephalopathy (SAE) in mice.
      Methods Eighteen male C57Bl/6 mice were randomly divided into a normal control group (group A), an SAE model group (group B), and a protein intervention group (group C), with 6 mice in each group. Group A received intraperitoneal injection of PBS; In group B and group C, SAE was induced in mice by intraperitoneal injection of LPS, the group B received intraperitoneal injection of PBS, while group C received intraperitoneal injection of PBS solution containing 5% AgB. The levels of anti-inflammatory factors interleukin-10 (IL-10), transforming growth factor-β (TGF-β), and pro-inflammatory factors tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by ELISA. The levels of liver and kidney function indicators in mice, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), serum creatinine (Cr) and urea (UREA), were detected using a fully automated biochemical analyzer. HE staining was used to observe the brain tissue damage in mice, and immunohistochemical staining was applied to detect the number of calcium-binding adapter molecule 1 (lba-1)-positive cells.
      Results Compared with group A, mice in group B had aggravated brain tissue damage, significantly increased levels of serum pro-inflammatory factors TNF-α and IL-6, decreased levels of anti-inflammatory factors IL-10 and TGF-β, increased levels of ALT, AST, CR, and UREA, and increased number of lba-1-positive cells in brain tissue (P < 0.01). Compared with group B, mice in group C showed reduced brain tissue damage, significantly decreased levels of serum pro-inflammatory factors TNF-α and IL-6, increased levels of anti-inflammatory factors IL-10 and TGF-β, decreased levels of ALT, AST, CR, and UREA, and reduced number of lba-1-positive cells in brain tissue (P < 0.01).
      Conclusions AgB has a protective effect on LPS-induced SAE in mice, which may be related to the inhibition of microglia activation.

       

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