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Hepato-cardiac axis in epirubicin toxicity: role of kynurenine pathway and N-acetylcysteine antioxidant intervention
(Wiley, 20/02/2026)
Epirubicin (EPI) is a widely used chemotherapeutic agent; however, its clinical utility is limited by severe side effects, particularly the production of reactive oxygen species (ROS). Among these, cardiotoxicity is one of the most critical issues, and it is worsened by impaired hepatic clearance resulting from liver dysfunction. This study aimed to investigate molecular changes induced by EPI in the liver within the kynurenine pathway (KP), their possible contribution to cardiotoxicity, and the protective effects of N-acetylcysteine (NAC). Rats received intraperitoneal injections of 50 or 300 mg/kg NAC, followed 1 h later by 9.6 mg/kg EPI. Tryptophan (Trp), kynurenine (Kyn), kynurenic acid (KYNA), quinolinic acid (QA), kynureninase, and kynurenine 3-monooxygenase (KMO) levels in the liver and cleaved caspase-3 levels in the liver and heart tissue were measured using ELISA. Hepatic and cardiac total antioxidant status (TAS) and total oxidant status (TOS) were determined using a colorimetric method. Plasma levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB), high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol (T-chol), and triglyceride (TG) were analyzed with a clinical biochemistry analyzer. Cardiac morphology was examined using hematoxylin-eosin staining. EPI administration was associated with increases in plasma CK-MB, the AST/ALT ratio, LDL, T-chol, and TG, with these increases partially attenuated by NAC treatment. Hepatic levels of Trp, QA, and KMO were positively correlated with plasma CK-MB and the AST/ALT ratio. Additionally, EPI appeared to increase oxidative stress in heart tissue and induce morphological changes. At the same time, NAC treatment was associated with partial improvement in these parameters, suggesting that alterations in the hepatic KP may be linked to possible cardiac involvement. Our findings suggest that EPI-induced alterations in hepatic KP may impair hepatic clearance, and NAC administration may provide partial protection, warranting further investigation of a possible hepato-cardiac interaction.
Effect of the hypothalamic serotonin on body weight change in the context of brain insulin resistance in Alzheimer’s disease
(Kastamonu Medical Journal, 16/06/2026) Ebru
Aims: The present work was designed to evaluate how alterations in serotonin (5-hydroxytryptamine, 5-HT), 5-HT receptor subtype 2B (5-HT2BR), and neuropeptide Y (NPY) are associated with body weight regulation in a rat model of brain insulin resistance (B-IR) that mimics the early pathological features of Alzheimer’s disease (AD).
Methods: B-IR was induced in rats through intracerebroventricular (i.c.v.) administration of amyloid-β₁–₄₂ oligomers at a dose of 2.5 nmol in a total volume of 10 μL. 5-HT concentrations were quantified in brainstem and hypothalamic samples, while hypothalamic levels of 5-HT2BR and NPY were determined using enzyme-linked immunosorbent assay (ELISA) methods. Body weight variation for each animal was defined as the difference between post-experimental and initial measurements. Group comparisons were conducted using the Mann–Whitney U test, and statistical significance was accepted at p < 0.05.
Results: Rats in the B-IR group showed a tendency toward increased 5-HT levels in brainstem tissue compared to the control group (p > 0.05), whereas hypothalamic 5-HT levels were significantly decreased in the B-IR group compared to controls (p < 0.01); body weight was significantly reduced in the B-IR group compared to the control group (p<0.01). In addition, rats in the B-IR group showed a downward trend in hypothalamic 5-HT2BR and NPY levels compared with the control group (p > 0.05 for both).
Conclusion: These findings suggest that decreased hypothalamic 5-HT levels in the B-IR group may be associated with the observed reduction in body weight. Additionally, the downward trends observed in 5-HT2BR and NPY levels may also be related to this change.
Epirubicin Alters Pancreatic Autophagy and Insulin Synthesis Through a Zinc-Dependent Mechanism
(Wiley, 12/06/2026) Ebru
Epirubicin (EPI) can cause metabolic side effects, including chemotherapy-related diabetes, partly through oxidative stress that disrupts zinc (Zn) homeostasis and impairs autophagy. This study investigated the effects of EPI on Zn regulation and autophagy in the pancreas, as well as the modulatory role of N-acetylcysteine (NAC). Rats received EPI (9.6 mg/kg) by intraperitoneal injection (i.p.) followed 1 h later by NAC (50 or 300 mg/kg, i.p.). Glucose homeostasis was assessed using the Homeostatic Model Assessment (HOMA-IR), and β-cell function was assessed using HOMA-β levels. Plasma insulin levels, as well as insulin, proinsulin, beclin, autophagy-related proteins (ATG5), Microtubule-Associated Protein 1 Light Chain 3 (LC3), phosphorylated Akt (p-Akt), mechanistic target of rapamycin complex 1 (mTOR1), cleaved caspase-3, Zrt/Irt-like Protein 10 (ZIP10), and the proliferation marker Ki-67 in pancreatic tissue, were measured using commercial ELISA kits. Total oxidant status (TOS) and total antioxidant status (TAS) were measured using commercial colorimetric assay kits, and the oxidative stress index (OSI) was calculated. Zn levels in pancreatic tissue and plasma samples were measured using a colorimetric method. Morphological changes in the pancreas were assessed by hematoxylin and eosin staining. As a result, in the EPI group, oxidative stress and ZIP10 levels increased, whereas Zn levels decreased, as well as pancreatic autophagy, proliferation, and insulin synthesis increased. Oxidative stress decreased in both the EN-50 and EN-300 groups, with a more pronounced decrease in the EN-300 group. Furthermore, in the EN-300 group, pancreatic Zn, ZIP10, autophagy, and proliferation levels decreased, whereas mTOR1 levels increased. The pancreatic insulin synthesis observed in the EN-50 group was not observed in the EN-300 group. In conclusion, the increased autophagy observed in the Epi group may reflect an adaptive response to oxidative stress. The effects of NAC on oxidative stress may be dose-dependent, and high-dose NAC administration may suppress EPI-induced autophagy via mTOR1-mediated signaling. Furthermore, the relationship among Zn levels, autophagy, and insulin synthesis observed in the experimental groups may contribute to a better understanding of EPI-associated diabetogenic alterations.
TURİST REHBERLİĞİ PROGRAMI(ÖRGÜN VE UZAKTAN)(2024-2025)
(2026)
KMYO.ÖZ.026.TURİST REHBERLİĞİ PROGRAMI(ÖRGÜN VE UZAKTAN)(2024-2025)
