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刺芒柄花素通过减轻细菌易位、炎症和氧化应激改善大鼠胃切除术后的肠黏膜屏障功能。

Calycosin Improves Intestinal Mucosal Barrier Function after Gastrectomy in Rats through Alleviating Bacterial Translocation, Inflammation, and Oxidative Stress.

作者信息

Peng Hui, Jin Lei, Zhang Qi, Shen Yi, Wang Zhen, Zhou Fuhai, Yu Qingsheng

机构信息

Department of General Surgery, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230031, Anhui, China.

出版信息

Evid Based Complement Alternat Med. 2022 Jun 26;2022:7412331. doi: 10.1155/2022/7412331. eCollection 2022.

DOI:10.1155/2022/7412331
PMID:35795283
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9251107/
Abstract

OBJECTIVE

Calycosin is the main bioactive extract of with anti-inflammation, antioxidant, and anticancer properties. Here, our study evaluated the protective effects and mechanisms of calycosin on intestinal mucosal barrier under gastrectomy.

METHODS

After receiving gastrectomy, the rats were administrated with 20 mg/kg, 40 mg/kg, or 80 mg/kg calycosin. Endotoxin, bacterial translocation, and intestinal bacterial flora were assayed. Intestinal injury was detected via hematoxylin and eosin staining. Tight junction indicators (occludin, claudin, and ZO-1) and apoptotic proteins (Bax, Bcl-2, and cleaved caspase 3) were examined in intestinal tissues. Inflammatory indicators (IL-1, IL-6, and TNF-) were examined in serum or intestinal specimens via ELISA. Apoptosis was assessed via TUNEL staining. IgA + B cells in intestinal tissues and sIgA in intestinal lumen were examined through immunohistochemistry and ELISA, respectively. Oxidative stress indicators (TSH, SOD, CAT, GSH-Px, and MDA) were also detected via ELISA.

RESULTS

Our results showed that calycosin administration decreased endotoxin levels in peripheral blood, intestine, and portal vein blood; lowered the bacterial translocation ratio; and regained the balance among intestinal bacterial flora (comprising bifidobacterium, lactic acid bacillus, enterobacter, enterococcus, aerobic bacteria, and anaerobic bacteria) in the rats with gastrectomy. After calycosin treatment, intestinal mucosal damage of the rats with gastrectomy was ameliorated, with the increase in expression of tight junction proteins. Additionally, calycosin reduced intestinal inflammation, apoptosis, secretion of sIgA, and oxidative stress in the rats with gastrectomy.

CONCLUSION

Altogether, our findings demonstrate that calycosin may improve intestinal mucosal barrier function under gastrectomy via reducing bacterial translocation, inflammation, and oxidative stress.

摘要

目的

毛蕊异黄酮是[具体植物名称]的主要生物活性提取物,具有抗炎、抗氧化和抗癌特性。在此,我们的研究评估了毛蕊异黄酮在胃切除术后对肠黏膜屏障的保护作用及机制。

方法

大鼠接受胃切除术后,分别给予20mg/kg、40mg/kg或80mg/kg的毛蕊异黄酮。检测内毒素、细菌移位和肠道菌群。通过苏木精-伊红染色检测肠道损伤。检测肠道组织中紧密连接指标(闭合蛋白、 Claudin蛋白和ZO-1)和凋亡蛋白(Bax、Bcl-2和裂解的半胱天冬酶3)。通过ELISA检测血清或肠道标本中的炎症指标(IL-1、IL-6和TNF-)。通过TUNEL染色评估细胞凋亡。分别通过免疫组化和ELISA检测肠道组织中的IgA+B细胞和肠腔中的分泌型IgA。还通过ELISA检测氧化应激指标(TSH、SOD、CAT、GSH-Px和MDA)。

结果

我们的结果表明,给予毛蕊异黄酮可降低外周血、肠道和门静脉血中的内毒素水平;降低细菌移位率;并恢复胃切除术后大鼠肠道菌群(包括双歧杆菌、乳酸杆菌、肠杆菌、肠球菌、需氧菌和厌氧菌)之间的平衡。毛蕊异黄酮治疗后,胃切除术后大鼠的肠黏膜损伤得到改善,紧密连接蛋白的表达增加。此外,毛蕊异黄酮还可减轻胃切除术后大鼠的肠道炎症、细胞凋亡、分泌型IgA分泌和氧化应激。

结论

总之,我们的研究结果表明,毛蕊异黄酮可能通过减少细菌移位、炎症和氧化应激来改善胃切除术后的肠黏膜屏障功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/864fef9f3457/ECAM2022-7412331.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/6aa5297711b4/ECAM2022-7412331.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/943e8f248983/ECAM2022-7412331.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/d66dc98c488a/ECAM2022-7412331.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/538fa88e31a7/ECAM2022-7412331.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/7126a9f83576/ECAM2022-7412331.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/c3737daced33/ECAM2022-7412331.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/864fef9f3457/ECAM2022-7412331.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/6aa5297711b4/ECAM2022-7412331.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/943e8f248983/ECAM2022-7412331.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/d66dc98c488a/ECAM2022-7412331.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/f81877b55c29/ECAM2022-7412331.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/538fa88e31a7/ECAM2022-7412331.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/7126a9f83576/ECAM2022-7412331.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/c3737daced33/ECAM2022-7412331.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/20b0/9251107/864fef9f3457/ECAM2022-7412331.008.jpg

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