European journal of pharmacology · 2025
Protective role of catechin hydrate against aluminum chloride-induced nephrotoxicity via oxidative stress, NF-κB, Bax/Bcl-2, and PERK-CHOP pathways.
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Yavuz Halil, Şimşek Hasan, Akaras Nurhan, Kandemir Özge, Tuncer Sibel Çiğdem, Kandemir Fatih Mehmet
Аннотация
AIM: Aluminum chloride (ALM) is a nephrotoxic compound that induces severe renal injury through oxidative stress, inflammation, apoptosis, and endoplasmic reticulum (ER) stress pathways. This study investigated the protective effects of catechin hydrate (CTH) against ALM-induced nephrotoxicity in male rats.
MATERIALS-METHODS: Thirty-five male Wistar rats divided into five groups: Control, ALM (100 mg/kg), CTH (20 mg/kg), ALM + CTH10 (ALM + CTH 10 mg/kg), and ALM + CTH20 (ALM + CTH 20 mg/kg), all administered orally for 21 days. Kidney and blood samples were collected on day 22. Renal function (urea, creatinine), oxidative stress (MDA, SOD, CAT, GPx, GSH), and the expression levels of genes related to apoptotic, inflammatory, and endoplasmic reticulum stress pathways (qRT-PCR) were analyzed. Histopathological (H&E) and immunohistochemical (KIM-1, Caspase-3) evaluations assessed tissue damage and apoptosis.
RESULTS: ALM increased urea, creatinine, MDA, ROS, NF-κB activation, pro-inflammatory mediators (TNF-α, IL-1β, iNOS, COX-2), apoptotic markers (Bax/Bcl-2, Apaf-1, caspase-3), and ER stress (GRP78, CHOP, ATF-6, PERK, IRE1), while reducing antioxidant defenses (SOD, CAT, GPx, GSH). CTH reversed these effects by restoring antioxidant balance, inhibiting NF-κB, reducing inflammation and apoptosis, and mitigating ER stress. Histological analyses confirmed CTH's protective role, lowering KIM-1 and Caspase-3 expression.
CONCLUSION: Overall, CTH modulates oxidative stress, inflammation, apoptosis, and ER stress, offering therapeutic potential against ALM-induced nephrotoxicity.
MATERIALS-METHODS: Thirty-five male Wistar rats divided into five groups: Control, ALM (100 mg/kg), CTH (20 mg/kg), ALM + CTH10 (ALM + CTH 10 mg/kg), and ALM + CTH20 (ALM + CTH 20 mg/kg), all administered orally for 21 days. Kidney and blood samples were collected on day 22. Renal function (urea, creatinine), oxidative stress (MDA, SOD, CAT, GPx, GSH), and the expression levels of genes related to apoptotic, inflammatory, and endoplasmic reticulum stress pathways (qRT-PCR) were analyzed. Histopathological (H&E) and immunohistochemical (KIM-1, Caspase-3) evaluations assessed tissue damage and apoptosis.
RESULTS: ALM increased urea, creatinine, MDA, ROS, NF-κB activation, pro-inflammatory mediators (TNF-α, IL-1β, iNOS, COX-2), apoptotic markers (Bax/Bcl-2, Apaf-1, caspase-3), and ER stress (GRP78, CHOP, ATF-6, PERK, IRE1), while reducing antioxidant defenses (SOD, CAT, GPx, GSH). CTH reversed these effects by restoring antioxidant balance, inhibiting NF-κB, reducing inflammation and apoptosis, and mitigating ER stress. Histological analyses confirmed CTH's protective role, lowering KIM-1 and Caspase-3 expression.
CONCLUSION: Overall, CTH modulates oxidative stress, inflammation, apoptosis, and ER stress, offering therapeutic potential against ALM-induced nephrotoxicity.