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Войти в исследования Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2026
Cisplatin-induced inflammatory liver injury via promoting free radicals' accumulation and Bax/Caspase-3 apoptotic signaling cascades: A possible mitigating role of high-purity selenium.
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Aboraya Dina M, Risha Engy F, El Baz Ayman, Rajab Bodour S, Albukhari Talat A, Filimban Waheed A, Sembawa Hatem, El-Sebaey Ahmed M, El-Boshy Mohamed E, Abdelhamid Fatma M
Аннотация
BACKGROUND: Cisplatin is a prevalent anti-tumor agent despite its association with DNA damage, oxidative stress, myelosuppression, and hepatotoxicity, which may limit its use. The current study aims to assess the mitigating effect of selenium on cisplatin-induced hepatotoxicity.
METHODS: Thirty-two adult albino rats were evenly divided into four groups: the control group received normal saline, the CIS group was IP injected with a single dose of cisplatin (7.5 mg/kg BW) on the 22nd day, the SE group received selenium (1 mg/kg BW, orally) for 21 days, and the SE + CIS group received selenium daily followed by a single IP dose of cisplatin. Samples were collected for hemogram, liver function tests, hepatic redox status, expression of pro- and anti-inflammatory cytokines, and evaluation of pro-apoptotic proteins.
RESULTS: In the CIS group, hepatobiliary enzymes, bilirubin, cholesterol, triglycerides, blood glucose, hepatic MDA, and TNF-α mRNA expression increased significantly (P ≤ 0.001) and correlated positively (r = 0.99-0.80) with hepatocyte necrosis, pro-apoptotic Bax, and Caspase-3 markers immunoreactivity. Total protein, albumin, globulin, SOD, CAT, GSH, and IL-10 expression significantly decreased (P ≤ 0.001) and correlated negatively (r = -0.99 to -0.80) with hepatopathies and pro-apoptotic marker expression. Indeed, hepatic damage scores and immunoreactivity for the pro-apoptotic markers Bax and caspase-3 were significantly ameliorated in the SE + CIS group. These mitigations showed strong correlations with improved liver function panel results, antioxidant capacity, and hepatocyte expression of IL-10 and TNF-α.
CONCLUSIONS: Pretreatment with selenium mitigates cisplatin-induced hepatocellular toxicity by promoting IL-10 expression, quenching free radicals, and activating downstream Bax/Caspase-3 apoptotic signaling cascades.
METHODS: Thirty-two adult albino rats were evenly divided into four groups: the control group received normal saline, the CIS group was IP injected with a single dose of cisplatin (7.5 mg/kg BW) on the 22nd day, the SE group received selenium (1 mg/kg BW, orally) for 21 days, and the SE + CIS group received selenium daily followed by a single IP dose of cisplatin. Samples were collected for hemogram, liver function tests, hepatic redox status, expression of pro- and anti-inflammatory cytokines, and evaluation of pro-apoptotic proteins.
RESULTS: In the CIS group, hepatobiliary enzymes, bilirubin, cholesterol, triglycerides, blood glucose, hepatic MDA, and TNF-α mRNA expression increased significantly (P ≤ 0.001) and correlated positively (r = 0.99-0.80) with hepatocyte necrosis, pro-apoptotic Bax, and Caspase-3 markers immunoreactivity. Total protein, albumin, globulin, SOD, CAT, GSH, and IL-10 expression significantly decreased (P ≤ 0.001) and correlated negatively (r = -0.99 to -0.80) with hepatopathies and pro-apoptotic marker expression. Indeed, hepatic damage scores and immunoreactivity for the pro-apoptotic markers Bax and caspase-3 were significantly ameliorated in the SE + CIS group. These mitigations showed strong correlations with improved liver function panel results, antioxidant capacity, and hepatocyte expression of IL-10 and TNF-α.
CONCLUSIONS: Pretreatment with selenium mitigates cisplatin-induced hepatocellular toxicity by promoting IL-10 expression, quenching free radicals, and activating downstream Bax/Caspase-3 apoptotic signaling cascades.