Bromelain diminishes renal consequences induced by gamma irradiation via suppressing ACE/Ang-II/aldosterone pathway in rats

Document Type : Original Article

Authors

1 Health Radiation Research Department, National Center for Radiation Research and Technology, Atomic energy authority

2 Health Radiation Research Department, National Center for Radiation Research and Technology,

3 health radiation research department, national center for radiation research and technology, atomic energy authority

Abstract

Radiation causes renal damage by enhancing the renin-angiotensin-aldosterone system's (RAAS) activation. This work aimed to evaluate the role of bromelain, an angiotensin-converting enzyme inhibitor (ACEI) in hindering the inflammatory and fibrotic impact of radiation via suppressing this pathway. Rats were subjected to a single dosage of 7.5 Gy then administered bromelain (30 mg/kg) orally for 14 days after one hour of irradiation. Gamma radiation caused a considerable increase in (RAAS) indices such as angiotensin II (AngII), aldosterone and angiotensin-converting enzyme (ACE) protein expression, in along with renal function: urea, creatinine and blood urea nitrogen with significant disturbance in oxidative stress markers: malondialdehyde (MDA), protein carbonyl (PCO), reduced glutathione (GSH), total thiol (tSH) and superoxide dismutase (SOD) in renal tissue homogenate. In addition, there was a notable increase in the renal inflammatory mediator's levels: tumor necrosis factor-α (TNF-α), nuclear factor kappa B (NF-κB) and interleukin-1β (IL-1β) alongside serum profibrotic markers: hyaluronic acid (HA), laminin (LN), type III procollagen (PCIII) and renal hydroxyproline (HYP) levels. Bromelain treatment dramatically improves the previously described parameters and modifies the radiation-induced renal histopathological damage in retaliation to the suppression of ACE, Ang II and aldosterone expressions.
Conclusions: Bromelain hinders radiation-induced inflammatory, fibrotic and oxidative stress response via remodelling the RAAS pathway in rats

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