الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Kidney injury (KI) is one of the most main causes of disability and mortality in several countries in the world. KI is caused when the kidneys are damaged and not functioning as they should. Heart and metabolic problems often accompany renal damage. Renin-angiotensin-aldosterone system’s (RAAS) overactivity, promotes vasoconstriction, hypertension, and renal inflammation, and is linked to the advancement of kidney disease. Nitric oxide (NO), being a vasodilator, is considered to play a significant role in the homeostatic regulation of renal hemodynamics in both normotensive and hypertensive states. Significantly, deficient renal NO synthesis in response to blockade of nitric oxide synthases by Nω -nitro-L-arginine methyl ester hydrochloride (L-NAME) outcomes in severe hypertension and progressive kidney damage when induced in male Wistar rats.The present study has focused on formulating β-carotene -loaded silica nanoparticles (βC-SiNPs) using post- and in situ-loading methods through synthesizing and characterizing SiNPs and βC-SiNPs with the modified Stober method. Our research was carried out to show–for the first time- the therapeutic potential of using a newly developed nanoformulation of a safe and stable βC-SiNPs as a targeted therapy to enhance the curability of acute kidney injury (AKI) through a comparative assessment between oral administration of nanoformulated βC and its native form as a renoprotective, hypolipidemic, antioxidant, and anti-inflammatory agents. L-NAME was administrated orally (40 mg/kg b.wt /day/2 weeks) for induction AKI in Wistar male rats. βC and βC-SiNPs were administrated orally (10 mg /kg b.wt/day/2 weeks) in the prevention of AKI.The current study demonstrated the amelioration effect of the βC-SiNPs on kidney, heart function, and oxidative stress-related to kidney disease in hypertensive-induced rats and detect its effect on the expression of Nrf2, HO-1, IL-6, Collagen IV, eNOS, iNOS, TNF-α, and mTOR. To the best of our knowledge, βC-SiNPs were more efficient as a renoprotective agent than their native form (βC) as the first comparative assessment between them.