Diclofenac predisposes benign prostate hyperplasia in fat feed albino rats
DOI:
https://doi.org/10.18203/2319-2003.ijbcp20220403Keywords:
Diclofenac, Fat, Hepatotoxicity, Haematology, PSAAbstract
Background: An attempt to establish the possible cause(s) of benign prostate hyperplasia (BPH) in fat feed albino rats treated with diclofenac (DCF)-potassium (K) was performed to ascertain its likely translational relationship in humans.
Methods: Thirty-five male wistar albino rats of 24 weeks old were divided into five groups of 7 animals each were used. Group 1; the normal control (NC) was injected subcutaneously with the vehicle (olive oil) only and served normal diet. Group 2; standard group treated with testosterone propionate in olive oil (3 mg/kg b. wt.). Groups 3, 4, and 5 were fed with the standard feed mixed with animal fat (sourced from roasted meat/condiments in aluminium foils) in 20, 40 and 80% portions, then treated with DCF-K in solution as low (2 mg/kg b. wt.), mid (4 mg/kg b. wt.), and high (6 mg/kg b. wt.) doses, respectively. The blood samples collected were analysed for prostate specific antigen (PSA), hematological parameters, kidney and liver function.
Results: Group 3 showed the highest PSA elevation (p<0.05) when compared to the control and the untreated group. There was a significant elevation (p<0.05) in WBC levels compared to all other groups. PCV, MCV, NEUT, MONO and EOSIN levels increased significantly (p<0.05) across all groups. Significant (p<0.05) increase was observed in liver and kidney parameters compared to the untreated groups. Significant (p<0.05) elevation in total cholesterol and LDL-C levels across the groups was observed. The DCF-K treated groups showed increase in several parameters compared to the untreated groups.
Conclusions: It was obvious that fatty diet and use of DCF-K contributed to the observed hepatotoxicity, nephrotoxicity, hence predisposed tissue damage and inflammation which conjunctly elevated PSA.
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