Data/hora: 08/06/2024 03:42:22

Provedor de dados: | 56
País: | Brazil
Título: | Captopril alleviates hypertension-induced renal damage, inflammation, and NF-κB activation
Autores: | Gan,Zhongyuan; Huang,Dan; Jiang,Jiaye; Li,Yuan; Li,Hanqing; Ke,Yan.
Data: | 2018-01-01
Ano: | 2018
Palavras-chave: | Captopril; Spontaneously hypertensive rats; Renal injury; Inflammation; Nuclear factor-κB.
Resumo: | Hypertensive renal damage generally occurs during the middle and late stages of hypertension, which is typically characterized by proteinuria and renal inflammation. Captopril, an angiotensin-converting enzyme (ACE) inhibitor, has been widely used for therapy of arterial hypertension and cardiovascular diseases. However, the protective effects of captopril on hypertension-induced organ damage remain elusive. The present study was designed to explore the renoprotective action of captopril in spontaneously hypertensive rats (SHR). The 6-week-old male SHR and age-matched Wistar-Kyoto rats were randomized into long-term captopril-treated (34 mg/kg) and vehicle-treated groups. The results showed that in SHR there was obvious renal injury characterized by the increased levels of urine albumin, total protein, serum creatinine, blood urea nitrogen, renal inflammation manifested by the increased mRNA and protein expression of inflammatory factors including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and inducible nitric oxide synthase, and enhanced nuclear factor-κB (NF-κB) activation. Captopril treatment could lower blood pressure, improve renal injury, and suppress renal inflammation and NF-κB activation in SHR rats. In conclusion, captopril ameliorates renal injury and inflammation in SHR possibly via inactivation of NF-κB signaling.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018001100602
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/1414-431x20187338
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.51 n.11 2018
Fonte: | info:eu-repo/semantics/openAccess