Ethanol Extract of Cosmos caudatus Attenuates Oxidative Stress and Inflammation in a Testosterone-Induced Benign Prostatic Hyperplasia Rat Model via Reduction of Malondialdehyde, Interleukin-6, and Tumor-Infiltrating Lymphocytes Activity
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Abstract
Benign Prostatic Hyperplasia (BPH) is a common age-related urological condition driven by chronic inflammation and oxidative stress, prompting the search for safer phytotherapeutic alternatives. This study evaluated the in vivo efficacy of ethanolic extract of Cosmos caudatus leaves in modulating the oxidative-inflammatory axis underlying testosterone-induced benign prostatic hyperplasia. Blood samples (0.5–1 mL) were collected from the retro-orbital plexus at baseline (T0), post-induction (T1), and post-treatment (T2) of thirty male Rattus norvegicus obtained from the Laboratory Animal Unit, Universitas Sebelas Maret, were allocated into five groups (n=6): Normal, Control, Positive Control receiving Finasteride, and treatment groups administered C. caudatus extract at 125 mg/kg or 250 mg/kg. BPH was induced using testosterone propionate (3 mg/kg/day, s.c.) for 28 days, followed by a 28-day treatment period. Serum malondialdehyde, interleukin-6, stromal tumor-infiltrating lymphocytes, prostate weight, and prostate index were evaluated. Testosterone induction significantly increased oxidative stress, systemic inflammation, and stromal lymphocytic infiltration, together with notable prostate enlargement (p<0.05). Treatment with both doses of C. caudatus extract markedly reduced malondialdehyde and interleukin-6 levels, suppressed tumor-infiltrating lymphocytes infiltration, and decreased prostate weight and prostate index compared with the untreated benign prostatic hyperplasia group (p<0.05), showing therapeutic effects comparable to Finasteride. These findings demonstrate that C. caudatus effectively attenuates benign prostatic hyperplasia progression through strong antioxidant and anti-inflammatory mechanisms, indicating its potential as a promising phytotherapeutic candidate targeting the oxidative-inflammatory axis in benign prostatic hyperplasia.
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