Shikimic acid recovers diarrhea and its complications in SD rats fed lactose diet to induce diarrhea.

IF 2.7 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Khaled M M Koriem, Alaa M A Abdeen
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引用次数: 0

Abstract

Background: Diarrhea is the increase of excretion of human water content and an imbalance in the physiologic processes of the small and large intestine while shikimic acid is an important biochemical metabolite in plants. This study aims to study the anti-diarrheal activity of shikimic acid through restoring kidney function, antioxidant activity, inflammatory markers, sodium/potassium-ATPase activity, apoptosis genes, and histology of the kidney in SD rats fed lactose diet to induce diarrhea.

Results: Thirty-six male SD rats (150 ± 10 g, 12 weeks old) were divided into 2 equal groups (18 rats/group) as follows: normal and diarrheal rats. Normal rats were divided into 3 equal groups of 6 rats each: the control, shikimic acid, and desmopressin drug groups. Diarrheal rats were also divided into 3 equal groups of 6 rats each: diarrheal, diarrheal rats + shikimic acid, and diarrheal rats + desmopressin drug groups. Shikimic acid restored serum urea and creatinine, urinary volume, kidney weight, sodium, potassium, and chloride balance in serum and urine. The acid returned the antioxidant (superoxide dismutase, glutathione peroxidase, catalase, malondialdehyde, NADPH oxidase activity, conjugated dienes, and oxidative index) activity and the inflammatory markers (tumor necrosis factor-α, interleukin-1β, interleukin-6, and interleukin-10) to values approaching the control values. Shikimic acid also restored the sodium/potassium-ATPase activity, the apoptosis genes p53 and bcl-2, and the histology of kidney tissue in diarrheal rats to be near the control group.

Conclusions: Shikimic acid rescues diarrhea and its complications through restoring kidney function, serum and urinary electrolytes, antioxidant activity, inflammatory markers, sodium/potassium-ATPase activity, the apoptosis genes, and the histology of the kidney in diarrheal rats to approach the control one.

食入乳糖饮食诱发腹泻的SD大鼠,其痢疾及其并发症可从石米酸中恢复。
背景:腹泻是指人体水分排泄量增加,小肠和大肠生理过程失衡,而莽草酸是植物中重要的生化代谢产物。本研究旨在通过恢复乳糖饮食诱导腹泻的SD大鼠的肾功能、抗氧化活性、炎症标志物、钠/钾ATP酶活性、凋亡基因和肾脏组织学来研究莽草酸的抗腹泻活性。结果:36只雄性SD大鼠(150只 ± 10g、12周龄)分为2组(18只/组):正常大鼠和腹泻大鼠。正常大鼠分为3组,每组6只:对照组、莽草酸组和去氨加压素药物组。腹泻大鼠也被分成3组,每组6只:腹泻大鼠、腹泻大鼠 + 莽草酸和腹泻大鼠 + 去氨加压素药物组。莽草酸可恢复血清尿素和肌酸酐、尿量、肾重量、血清和尿液中的钠、钾和氯平衡。该酸使抗氧化剂(超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶、丙二醛、NADPH氧化酶活性、共轭二烯和氧化指数)活性和炎症标志物(肿瘤坏死因子-α、白细胞介素-1β、白细胞素-6和白细胞介质-10)恢复到接近对照值的值。莽草酸还使腹泻大鼠的钠/钾ATP酶活性、凋亡基因p53和bcl-2以及肾组织的组织学恢复到接近对照组。结论:通过恢复腹泻大鼠的肾功能、血清和尿液电解质、抗氧化活性、炎症标志物、钠/钾ATP酶活性、细胞凋亡基因和肾脏组织学等指标,与对照组相比,莽草酸可以挽救腹泻及其并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
4.40
自引率
0.00%
发文量
32
审稿时长
8 weeks
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