Aqueous garlic extract supresses experimental gentamicin induced renal pathophysiology mediated by oxidative stress, inflammation and Kim-1.
Pathophysiology
; 26(3-4): 271-279, 2019.
Article
en En
| MEDLINE
| ID: mdl-31383388
BACKGROUND: Gentamicin (Gent) has rapid & high bactericidal action in addition to its cheap price. Nevertheless, 30% of gentamicin-treated patients develop nephrotoxicity. OBJECTIVE: To explore the probable nephroprotective effects of the aqueous garlic extract (AGE) & to elucidate its underlying mechanisms via monitoring proinflammatory cytokines as tumer necrosis factor (TNF-α), interleukin 6 (IL-6) and interferon-γ (INF-γ), oxidative stess markers as malondialdehyde (MDA) & superoxide dismutase (SOD) & kidney injury molecule (Kim-1) as a promising early specific biomarker of renal dysfunction. METHODS: 32 adult male rats were divided into 4 equal groups treated for 21 days as: normal control group received normal saline orally, AGE-treated group received AGE at 250â¯mg/kg/day orally, Gent-treated group received Gent-sulphate intraperitoneal injection at 80â¯mg/kg /day, and AGE & Gent cotreated group received AGE and Gent concomitantly in the same previous doses. Serum urea, creatinine, glomerular filteration rate (GFR), systolic (SBP) and diastolic blood pressure (DBP), TNF-α, IL-6, INF-γ, MDA and SOD and Kim-1 mRNA expression were evaluated in kidney tissue homogenate. Renal cortex sections stained with Haematoxylin & eosin (H&E) were examined. RESULTS: AGE is nephroprotective through significantly reducing serum urea, creatinine, SBP and DBP, TNF-α, IL-6, INF-γ and MDA (the main product of lipid peroxidation), decreasing expression of Kim-1 mRNA in renal tissue and increasing level of GFR, the natural antioxidant SOD and improving renal histological features of Gent-treated rats. CONCLUSION: AGE normalizes Gent-induced renal dysfunction. Their co-administration is a plausible advice, although the therapeutic efficiency of Gent was not investigated.
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01-internacional
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MEDLINE
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En
Revista:
Pathophysiology
Año:
2019
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Article
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