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益生菌对脂多糖诱导的大鼠实验性脓毒症模型心脏损伤的保护作用

Protective Effect of Probiotics on Cardiac Damage in Experimental Sepsis Model Induced by Lipopolysaccharide in Rats.

作者信息

Taş Necip Gökhan, Aktaş Osman, Taş Hakan Gökalp, Zırh Selim, Kurt Nezahat, Uslu Hakan

机构信息

Experimental Animal Application and Research Center, Erzincan Binali Yıldırım University, Erzincan 24002, Turkey.

Department of Medical Microbiology, Faculty of Medicine, Ataturk University, Erzurum 25030, Turkey.

出版信息

Medicina (Kaunas). 2025 Mar 25;61(4):589. doi: 10.3390/medicina61040589.

Abstract

: Probiotics have been shown to be effective in controlling various adverse health conditions such as antibiotic-associated diarrhea, inflammatory bowel disease, obesity, and neurological diseases. However, to our knowledge, there is no research on the preventive effect of probiotics on heart damage caused by infections. This study examined the preventive benefits of probiotics against sepsis-related heart injury using a rat model caused by lipopolysaccharide (LPS). : Four groups of twenty-four male Wistar albino rats, each with six rats, were set up. For 14 days, Group 1 (Sham Group) was given oral normal saline, intraperitoneal O111-B4 lipopolysaccharide (LPS Group) was given to Group 2, and oral probiotics were given to Group 3 (Probiotic Group). O111-B4 lipopolysaccharide was injected intraperitoneally after Group 4 (Probiotic + LPS) received oral probiotics containing GG and subsp. BB-12 (10 CFU/day). Blood samples were taken twenty-four hours following the administration of LPS. The animals were then euthanized by cervical dislocation, and samples of cardiac tissue were taken in order to assess any damage to the heart. The following serum values were measured: C-reactive protein (CRP), creatine kinase-myocardial band (CK-MB), cardiac troponin subunit I (cTn-I), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6). The TNF-α, IL-1β, IL-6, glutathione (GSH), malondialdehyde (MDA), Total Oxidant Status (TOS), Total Antioxidant Status (TAS), Oxidative Stress Index (OSI), CRP, CK-MB, and cTn-I levels were assessed in tissue samples. Additionally, staining techniques were used to analyze histopathological alterations in tissues. : With the exception of serum IL-6 ( = 0.111), tissue and serum cytokine levels were considerably greater in the sepsis group (Group 2) than in the other groups ( < 0.05 to <0.001). The TAS, GSH, and SOD levels were significantly lower ( < 0.05 to <0.001) in septic rats, although the tissue levels of TOS, OSI, and MDA were significantly higher. With the exception of serum CRP in Group 3 ( = 0.328), the CK-MB, CRP, and cTn-I levels were considerably higher in Group 2 than in the other groups ( < 0.01 to <0.001). When compared to the other groups, histopathological examination showed significant alterations in the LPS group. : Probiotics showed positive effects on oxidative stress markers and dramatically decreased sepsis-induced cardiac damage in the LPS-induced sepsis model. These results imply that probiotics could be used as a therapeutic approach to lessen the cardiac damage brought on by sepsis.

摘要

益生菌已被证明在控制各种不良健康状况方面有效,如抗生素相关性腹泻、炎症性肠病、肥胖症和神经疾病。然而,据我们所知,尚无关于益生菌对感染所致心脏损伤预防作用的研究。本研究使用脂多糖(LPS)诱导的大鼠模型,检测了益生菌对脓毒症相关心脏损伤的预防益处。

将四组共24只雄性Wistar白化大鼠,每组6只,进行分组。第1组(假手术组)连续14天口服生理盐水,第2组(LPS组)腹腔注射O111 - B4脂多糖,第3组(益生菌组)口服益生菌。第4组(益生菌 + LPS组)口服含GG和亚种BB - 12(10 CFU/天)的益生菌后腹腔注射O111 - B4脂多糖。在给予LPS 24小时后采集血样。然后通过颈椎脱臼法对动物实施安乐死,并采集心脏组织样本以评估心脏损伤情况。检测以下血清值:C反应蛋白(CRP)、肌酸激酶心肌型(CK - MB)、心肌肌钙蛋白I亚基(cTn - I)、肿瘤坏死因子 - α(TNF - α)、白细胞介素 - 1β(IL - 1β)和白细胞介素 - 6(IL - 6)。评估组织样本中TNF - α、IL - 1β、IL - 6、谷胱甘肽(GSH)、丙二醛(MDA)、总氧化剂状态(TOS)、总抗氧化剂状态(TAS)、氧化应激指数(OSI)、CRP、CK - MB和cTn - I水平。此外,采用染色技术分析组织中的组织病理学改变。

除血清IL - 6(P = 0.111)外,脓毒症组(第2组)的组织和血清细胞因子水平显著高于其他组(P < 0.05至P < 0.001)。脓毒症大鼠的TAS、GSH和超氧化物歧化酶(SOD)水平显著降低(P < 0.05至P < 0.001),而组织中的TOS、OSI和MDA水平显著升高。除第3组血清CRP(P = 0.328)外,第2组的CK - MB、CRP和cTn - I水平显著高于其他组(P < 0.01至P < 0.001)。与其他组相比,组织病理学检查显示LPS组有显著改变。

在LPS诱导的脓毒症模型中,益生菌对氧化应激标志物显示出积极作用,并显著降低了脓毒症诱导的心脏损伤。这些结果表明,益生菌可作为一种治疗方法来减轻脓毒症所致的心脏损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acb8/12029071/f84c8e877a11/medicina-61-00589-g001a.jpg

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