Boswellic Acid and Carnosine Ameliorate Vanadyl-Sulfate-Induced Renal Damage via Regulating Nrf2/HO-1 and PI3K/AKT Pathways.

IF 3.6 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Ghada M Gad, Nahla S Kotb, Khalid S Hashem
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引用次数: 0

Abstract

Nephrotoxicity is a condition caused by the negative effects of several chemotherapy treatments on the kidneys. Our target was to determine how boswellic and carnosic acids protected rats against vanadyl sulfate (VOS)-induced nephrotoxicity. A total of 30 male Wistar albino rats were used in the investigation. They were divided into sex groups (five rats in each group) as follows: Rats in the control group were given carboxymethyl cellulose (CMC) at a concentration of 0.5%. VOS group was administered a weekly intraperitoneal injection of VOS 50 mg/kg for six consecutive weeks. For 6 weeks in a row, rats in the boswellic acid group were given injections of BA every day at a dose of 100 mg/kg orally. Group receiving carnosic acid received 100 mg/kg of CA orally daily for 6 consecutive weeks. For 6 weeks, rats in the boswellic acid plus VOS group were given 50 mg/kg of VOS intraperitoneally (i.p.) once a week and 100 mg/kg of BA orally daily. For 6 weeks, the carnosic acid plus VOS group received 50 mg/kg of VOS intraperitoneally once a week and 100 mg/kg of CA orally daily. In contrast to the control group, our results demonstrated that the injection of vanadyl sulfate to the VOS group contributed a significant increase in creatinine and blood urea as well as disordered kidney oxidative antioxidant interaction. The injection of vanadyl sulfate to the VOS group produced an increase in renal MDA concentration and a decrease in renal SOD activity, GSH content, GR, and CAT activities in comparison to the control group. When compared to the control group, our study on renal mRNA expression revealed that administering vanadyl sulfate to the VOS group increases renal iNOS, PI3K, and AKT mRNA expressions and modulates the mRNA expression of renal Nrf2 and HO-1. According to the current investigation, treating rats with BA or CA can reduce their nephrotoxicity from VOS; when the defective kidney oxidative antioxidant redox levels were returned to normal, the fibrosis in the Van-treated animals decreased. These findings are consistent with interactions between the Pi3k/Akt and Nrf2/Ho-1 pathways, as one of the human body's most vital organs.

乳香酸和肌肽通过调节Nrf2/HO-1和PI3K/AKT通路改善硫酸钒诱导的肾损伤。
肾毒性是由几种化疗对肾脏的负面影响引起的一种情况。我们的目的是确定乳香酸和鼠尾草酸如何保护大鼠免受硫酸钒基(VOS)引起的肾毒性。实验选用雄性Wistar白化大鼠30只。按性别分组,每组5只大鼠:对照组大鼠给予浓度为0.5%的羧甲基纤维素(CMC);VOS组大鼠每周腹腔注射VOS 50 mg/kg,连续6周。乳香酸组大鼠连续6周,每天口服100 mg/kg剂量的BA。鼠尾草酸组给予100 mg/kg CA,每日口服,连续6周。乳香酸加VOS组大鼠给予VOS 50 mg/kg腹腔灌胃,每周1次,BA 100 mg/kg口服,持续6周。鼠尾草酸加VOS组每周腹腔注射VOS 50 mg/kg,每天口服CA 100 mg/kg,持续6周。与对照组相比,我们的研究结果表明,向VOS组注射硫酸钒酯导致肌酐和血尿素显著增加,肾脏氧化抗氧化相互作用紊乱。与对照组相比,VOS组注射硫酸钒使肾脏MDA浓度升高,肾脏SOD活性、GSH含量、GR和CAT活性降低。与对照组相比,我们对肾脏mRNA表达的研究发现,VOS组给予硫酸钒酯增加了肾脏iNOS、PI3K和AKT mRNA的表达,并调节了肾脏Nrf2和HO-1的mRNA表达。根据目前的研究,BA或CA治疗大鼠可减轻VOS肾毒性;当缺陷肾的氧化抗氧化氧化还原水平恢复正常时,van处理的动物的纤维化减少。这些发现与Pi3k/Akt和Nrf2/Ho-1通路之间的相互作用是一致的,Nrf2/Ho-1通路是人体最重要的器官之一。
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
Biological Trace Element Research
Biological Trace Element Research 生物-内分泌学与代谢
CiteScore
8.70
自引率
10.30%
发文量
459
审稿时长
2 months
期刊介绍: Biological Trace Element Research provides a much-needed central forum for the emergent, interdisciplinary field of research on the biological, environmental, and biomedical roles of trace elements. Rather than confine itself to biochemistry, the journal emphasizes the integrative aspects of trace metal research in all appropriate fields, publishing human and animal nutritional studies devoted to the fundamental chemistry and biochemistry at issue as well as to the elucidation of the relevant aspects of preventive medicine, epidemiology, clinical chemistry, agriculture, endocrinology, animal science, pharmacology, microbiology, toxicology, virology, marine biology, sensory physiology, developmental biology, and related fields.
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