Hesperidin dietary intervention mitigates ammonia stress-evoked biochemical and metabolic disruption and restores the tlr-5–nf-κβ/mapk gene expression in Oreochromis niloticus

Nigella sativa oil ameliorates malathion-ınduced toxicity in Nile tilapia: a multi-systemic and molecular evaluation

Dietary supplementation of Acer truncatum leaf extract alleviates oxidative-stress induced impairment of ovarian function in laying hens via Nrf2-mediated antioxidant defense and VEGF-mediated angiogenesis

This study aimed to evaluate the potential of Acer truncatum leaf extract (ATLE) to mitigate oxidative-stress–induced impairment of reproductive function in laying hens, with a focus on mechanisms involving antioxidant defense, angiogenesis, and ovarian microenvironment homeostasis. Oxidative stress was induced by tert-butyl hydroperoxide (tBHP) injection. Hens were randomly assigned to a control group (CON), an oxidative stress group (BCON), and an oxidative stress group supplemented with 0.6% ATLE (BATLE). Egg-laying performance, ovarian morphology, reproductive hormones, oxidative stress markers, and angiogenesis indicators were evaluated and integrated with transcriptomic analysis. The results were as follows: 1) Production and Morphology: ATLE supplementation alleviated (P < 0.05) the tBHP-induced decrease in egg laying rate and elevation in feed conversion ratio (FCR). It also mitigated (P < 0.05) reductions in the number of hierarchical follicles and the ovarian stroma index while restoring (P < 0.05) serum concentrations of LH and GH, thereby re-establishing reproductive endocrine balance. 2) Antioxidant Defense: ATLE activated (P < 0.05) Nrf2 and increased (P < 0.05) transcription of downstream antioxidant genes, including SOD3, GPX3, PRDX4, GSR and CAT, thereby enhancing (P < 0.05) the SOD and CAT activities and reducing (P < 0.05) MDA concentrations within both serum and ovarian tissues. 3) Vascular Network Support: ATLE attenuated (P < 0.05) the tBHP-induced downregulation of angiogenic factors, including protein levels of VEGF, ANGPT1, and HIF-1α and mRNA expression levels of VEGFA, ANGPT1, ANGPT2, ITGA5, and MMP9. 4) Microenvironment Remodeling: Transcriptomic integration revealed that ATLE-mediated repair overlapped (> 88%) with oxidative-stress–induced damage across functional modules. By reversing dysregulation of key genes such as VEGFA, KDR, and FN1, ATLE restored core pathways including focal adhesion and ECM–receptor interaction, and coordinated processes such as extracellular matrix, angiogenesis, and response to wounding, driving a systemic remodeling of the ovarian reproductive microenvironment toward homeostasis. In summary, this study demonstrated that ATLE activated multiple signaling axes, notably Nrf2 and VEGF. As a result, ATLE enhanced antioxidant defenses against oxidative damage and promoted vascular health and microenvironmental remodeling in the ovary. Together, these effects preserved the structural integrity and function of the laying hen reproductive system. These findings supported the potential of ATLE as a natural feed additive and provided a scientific rationale for using nutritional strategies to alleviate oxidative stress and improve reproductive health in laying hens.

Toxic effects of MPs and Up Grade® herbicide on the Nile tilapia (Oreochromis niloticus): Oxidative stress, immune responses, and histopathological investigations

Zingerone Alleviates Acetaminophen‐Induced Liver Damage by Regulating Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy

The aim of this study is to investigate the protective effect of zingerone (ZNG), an antioxidant agent, against acetaminophen (APAP)‐induced liver damage, which is used as an analgesic and antipyretic. For this purpose, twenty‐eight male rats were divided into four groups: control, ZNG, APAP, and APAP + ZNG. ZNG was administered orally for 7 days, followed by a single dose of APAP on the 7th day. At the end of the study, biochemical, molecular, and immunohistochemical analyses were performed on the liver tissue. According to the data obtained, APAP was found to trigger oxidative stress, inflammation, autophagy, apoptosis, endoplasmic reticulum stress, autophagy, and heat shock proteins in liver tissue. On the other hand, it has been observed that after ZNG treatment, the activities of antioxidant enzymes SOD, GPx, and CAT increased, MDA levels, a significant indicator of lipid peroxidation, decreased, and GSH stores were replenished. Following ZNG treatment, apoptosis was attenuated, resulting in decreased mRNA transcript levels of Bax, caspase‐3, and increase in Bcl‐2 levels. ZNG treatment resulted in a decrease in endoplasmic reticulum stress, inflammation, autophagy mRNA transcript levels. In addition, a decrease in heat shock proteins was detected. In conclusion, it has been observed that ZNG may be a significant protective against APAP liver damage.

Dietary banana peels modulate waterborne oxyfluorfen-induced hepatotoxicity in Nile tilapia (Oreochromis niloticus) via regulation of redox homeostasis and ER stress signaling

Dexpanthenol Attenuates High-Fructose Corn Syrup-Induced Hepatic Injury in Young Adult Rats by Modulating Oxidative Stress, Apoptosis, and Inflammasome-Associated Pyroptotic Signaling

Excessive intake of high-fructose corn syrup (HFCS) contributes to pediatric metabolic dysfunction-associated steatotic liver disease, but the mechanisms linking fructose exposure to inflammatory cell death remain incompletely defined. This study investigated whether dexpanthenol (DEX) attenuates HFCS-induced liver injury by modulating oxidative stress, apoptosis, and nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome-associated pyroptotic signaling. Thirty-two young adult male Wistar rats were assigned to control, HFCS, HFCS+DEX, and DEX groups (n = 8 each). HFCS-induced liver injury was established with 20% HFCS-55 in drinking water for 8 weeks. DEX (500 mg/kg/day, intraperitoneally) was administered from the end of week 4 to week 8. Liver tissues were assessed by histopathology; immunohistochemistry for caspase-3, malondialdehyde, and proliferating cell nuclear antigen; biochemical measurement of total antioxidant and oxidant status; and RT-qPCR analysis of Nlrp3, caspase-1, gasdermin D, and interleukin-1β. HFCS exposure caused steatosis, inflammation, and necrosis; increased histopathological scores; enhanced caspase-3, malondialdehyde, and proliferating cell nuclear antigen expression; elevated total oxidant status; and markedly upregulated inflammasome-related genes. Total antioxidant status did not differ among groups. DEX significantly improved hepatic architecture; reduced immunohistochemical markers of oxidative stress, apoptosis, and injury-associated proliferation; and downregulated NLRP3, caspase-1, gasdermin D, and interleukin-1β expression. These findings suggest that DEX attenuates HFCS-induced liver injury through a multi-target mechanism involving suppression of oxidative damage, apoptosis, and inflammasome-associated pyroptotic signaling in young adult rats.