Involvement of redox status and the nuclear-related factor 2 in protecting against cadmium-induced renal injury with Sana Makki (Cassia senna L.) pre-treatment in male rats
Título del documento: Involvement of redox status and the nuclear-related factor 2 in protecting against cadmium-induced renal injury with Sana Makki (Cassia senna L.) pre-treatment in male rats
Revista: Anais da Academia Brasileira de Ciencias
Base de datos: PERIÓDICA
Número de sistema: 000436090
ISSN: 0001-3765
Autores: 1
2
3
4
1
5
4
Instituciones: 1King Saud University, College of Science, Riyadh. Arabia Saudita
2Princess Nourah bint Abdulrahman University, College of Health and Rehabilitation Science, Riyadh. Arabia Saudita
3Princess Nourah bint Abdulrahman University, College of Science, Riyadh. Arabia Saudita
4King Saud University, College of Science, Riyadh. Arabia Saudita
5Taif University, College of Applied Medical Science, Taif. Arabia Saudita
Año:
Volumen: 92
Número: 2
País: Brasil
Idioma: Inglés
Tipo de documento: Artículo
Enfoque: Aplicado, descriptivo
Resumen en inglés This study was designed to investigate the potential defensive strategy of Sana Makki extract (SME) against Cd-induced in vivo nephrotoxicity and its underlying mechanisms. Male albino rats were used in a thirty days study comparing control, SME-treated, CdCl2-treated, and combined SME and Cd treatment. Pre-treatment with SME significantly reduced serum kidney biomarkers (urea and creatinine), the concentration of renal KIM-1, and kidney index values. Additionally, SME also attenuated CdCl2-induced oxidative and nitrosative stress in renal tissue; significantly reducing malondialdehyde (MDA) and nitric oxide (NO) concentrations and significantly increasing antioxidant enzymes in kidney tissue. Molecularly, SME significantly upregulated antioxidant gene expression (SOD2, GR, GPx1, and CAT) caused by Cd. Notably, the augmented mRNA expression of nuclear-related factor 2 (Nrf2) by Cd was enhanced by SME administration. SME markedly suppressed the Cd-induced rise in pro-inflammatory cytokines. The combination of Cd and SME relieved the Cd-induced apoptotic damage by enhancing Bcl2 and suppressing Bax and Cas-3 levels in renal tissue. The renal tissue histoarchitecture confirmed the biochemical and molecular findings. Collectively, our data indicate that SME can counteract Cd-induced renal intoxication through anti-oxidative, anti-inflammatory, and anti-apoptotic mechanisms
Disciplinas: Medicina
Palabras clave: Farmacología,
Nefrología,
Cadmio,
Nefrotoxicidad,
Apoptosis,
Estrés oxidativo,
Efecto protector,
Cassia senna,
Fabaceae
Keyword: Pharmacology,
Nephrology,
Cadmium,
Nephrotoxicity,
Apoptosis,
Oxidative stress,
Protective effect,
Cassia sena,
Fabaceae
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