Abstract: Wheat germ oil (WGO) is a well-known product with anti-inflammatory and antioxidant
properties. The current study aimed to investigate the impacts of WGO against ethanol-induced
liver and kidney dysfunction at the serum, anti-inflammatory, antioxidants and anti-apoptotic signaling
pathways. Rats received saline orally as a negative control or WGO in a dose of 1.5 mL/kg
(1400 mg/kg body weight orally) for 15 days. The affected group received ethanol 50% v/v
10 mL/kg (5 g/kg) body weight orally once a day for consecutive 15 days to induce hepatorenal
injuries in ethanolic non-treated group. The protective group received WGO daily 1 h before
ethanol administration. Serum (1.5 mL) from blood was extracted and examined for the changes in
biochemical assessments in serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), bilirubin,
serum
-glutamyl transpeptidase (GGT), total protein, serum albumin, butyrylcholinesterase
(BChE), total cholesterol (TC), total triglyceride (TG), urea, creatinine, uric acid, potassium (K+),
Beta-2 microglobulin (2M), malondialdehyde (MDA), catalase (CAT), reduced glutathione (GSH),
superoxide dismutase (SOD) and aspartate aminotransferase (AST). Kidney and liver homogenate
was used to measure MDA, GSH and catalase activities. Quantitative real time PCR (qRT-PCR)
was used to express Nrf2 and HO-1 in liver, and NF-kB and kidney injury molecule (KIM-1) in
kidneys, which are correlated with oxidative stress and inflammation. Capase-3 and Bcl2 genes
were examined using immunohistochemical analysis in the kidney and liver. Ethanol administration
induced significant alteration in examined liver and kidney markers (AST, ALT, GGT, ALP, total
proteins, urea, creatinine and uric acid). Moreover, alcohol administration decreased antioxidant
activities at serum and hepatorenal tissues (GSH, catalase and SOD), while MDA was increased as a
tissue degradation marker. Inflammatory cytokines, together with genes of oxidative stress markers
(Nrf2 and HO-1), were all affected. At cellular levels, apoptotic marker caspase-3 was upregulated,
while antiapoptotic marker B-cell lymphoma 2 (Bcl2), was down regulated using immunohistochemical
analysis. Of interest, pretreatment with WGO improved the side effects induced by ethanol
on hepatic, renal biomarkers and reversed its impact on serum and tissue antioxidant parameters.
Nrf2/HO-1 were upregulated, while NFk-B and KIM-1 were downregulated using real time PCR.
Immune reactivities of caspase-3 and Bcl2 genes were restored in the protective group. In conclusion, |