Protective effect of royal jelly against diclofenac-induced hepato-renal damage and gastrointestinal ulcerations in rats

Abstract

Evaluation of traditionally used royal jelly (RJ) for the management of hepato-renal damage and gastrointestinal ulcerations caused by diclofenac. Methods: Forty adult male Wistar rats were allocated into four groups. Rats of the 1 st group received only saline and served as normal group. The remaining 3 groups received diclofenac (50 mg/kg/day, I.P.) for 7 days. Group 2 served as diclofenac-control group. Groups 3 and 4 received RJ (150 and 300 mg/kg/day, P.O.) respectively for 30 days. Twenty-four hours after the last treatment, blood samples were collected, rats were sacrificed, and livers, kidneys, stomachs & intestines were harvested. Stomachs and intestines were tested for ulcer counts. Serum levels of AST, ALT, creatinine and urea were investigated. Hepatic, renal, gastric and intestinal tissue contents of myeloperoxidase (MPO) and prostaglandin-E2 (PGE2) were measured. Histopathological examinations were also performed followed by immunohistochemical determination of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression. Results: Diclofenac administration caused significant deterioration of all the above mentioned parameters. RJ improved hepatic and renal functions. Gastric and intestinal ulcer counts were significantly ameliorated. Hepatic, renal, gastric and intestinal tissue PGE-2 contents and COX-2 expression were significantly elevated. RJ also significantly reduced MPO content and iNOS expression as compared to diclofenac-control group. Improvements of the histopathological pictures of hepatic, renal, gastric and intestinal tissues were also apparent. Conclusion:The study demonstrates promising protective effects of RJ against diclofenac-induced hepato-renal damage and gastrointestinal ulceration in rats.

Low-Phosphate Processed Cheese Diminishes Diclofenac-Induced Hepato-Renal Injury in Male Rats

“…Renal sections from animals subjected to group G-7 had typical histopathological order similar to that described to the diclofenac control group (G-2). Our findings were similar to those reported previously by Mostafa et al (2020) for kidneys of normal and DF-treated animals. The authors reported that renal sections from DF-treated rats showed massive areas of fibrosis and ongoing cell apoptosis.…”

“…Also, the formation of intensive mesangial matrix and widespread necrosis of the renal tubules could be detected easily. The formation of necrosis of the renal tubules is leading to dilatation of renal vessels, desquamation of tubular cells, the formation of the intraluminal cast, and infiltration of inflammatory leukocytes (Mostafa et al, 2020). Renal sections from animals subjected to group G-7 had typical histopathological order similar to that described to the diclofenac control group (G-2).…”

“…This harmful defect was remarkable particularly in animals subjected to treatments G-2 and G-7. Similarly, Mostafa et al (2020) reported that the administration of diclofenac (50-300 mg/kg) could result in elevation of serum creatinine and urea up to 272% and 217% respectively as compared to the normal control group. The elevation of creatinine and urea in the blood of DF-T animals indicated that diclofenac compromised the integrity of the glomerular filtration rate barrier, leading to impaired renal function (Farombi et al, 2002;Maalej et al, 2017).…”

Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response

“…The considerable elevation in the amount of creatinine, urea, and uric acid after exposure of rats to DIC may be a sign of kidney impairment. These findings suggested that probably DIC leads to a reduction in GFR of the animals, which in turn caused the elevation in the serum levels of some biochemical marker [ 34 , 35 , 36 ]. On the other hand, when CAR could diminish the serum levels of Cr, urea, and uric acid in rats after exposure to DIC, it could be assumed that probably this agent might have an ameliorative effect on DIC-induced nephrotoxicity through increasing GFR.…”

Royal Jelly and Aliskiren mutually annul their protective effects against gentamicin-induced nephrotoxicity in rats

“…with ALK (dissolved in normal saline at a dose of 50 mg/kg/day) for 30 min before the injection of GM [ 11 ]; and IV. GM+ALK+RJ group: The rats were administered orally with RJ (dissolved in normal saline at a dose of 150 mg/kg/day) [ 17 ] together with i.p. ALK (50 mg/kg/day) 30 min before GM injection.…”