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The poultry industry struggles with oxidative stress affecting gut health and productivity. This study examined using 1-Deoxynojirimycin (DNJ) extracts from mulberry leaves as an antioxidant in broilers feed to combat this issue. We divided 240 broilers, aged 16 days, into six groups, including a control and groups exposed to oxidative stress through HO injections, with different supplement levels of DNJ-E (40, 80, 120, and 160 mg/kg of the basal diet) lasting until the broilers reached 42 days old. We evaluated intestinal morphology, ultrastructure, oxidative stress markers, the tight junction, and inflammatory cytokines. Adding 40 mg/kg DNJ-E improved villus height, the villus-to-crypt ratio, and cellular ultrastructure, and increased SOD levels in the jejunum and ileum, as well as CAT levels in the duodenum and jejunum ( < 0.05), compared to the HO group. The addition of DNJ had differential effects on oxidative stress, the intestinal barrier, and immune-related genes. Importantly, the dosages of 40 mg/kg and 80 mg/kg resulted in an upregulation of mRNA expression ( < 0.05). These findings suggest that DNJ-E holds potential as a beneficial feed additive for enhancing broiler health, particularly at supplementation levels below 80 mg/kg, as higher concentrations may negatively influence intestinal health. Future investigations should aim to elucidate the underlying mechanisms through which DNJ-E operates within the avian gastrointestinal system.
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http://dx.doi.org/10.3390/ani14223319 | DOI Listing |
Neurochem Res
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Biology and Health Laboratory, Faculty of Sciences, Ibn Tofail University, Kenitra, Morocco.
Parkinson's disease (PD) is characterized by impairments in motor control following the degeneration of dopamine-producing neurons located in the substantia nigra pars compacta. Environmental pesticides such as Paraquat (PQ) and Maneb (MB) contribute to the onset of PD by inducing oxidative stress (OS). This study evaluated the therapeutic efficacy of moderate physical activity (PA) on both motor and non-motor symptoms in a Wistar rat model of Paraquat and Maneb (PQ/MB) induced PD.
View Article and Find Full Text PDFMol Biol Rep
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Behbahan Faculty of Medical Sciences, Behbahan, Iran.
Metab Brain Dis
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Department of Neuroscience, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
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View Article and Find Full Text PDFCell Biochem Biophys
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Faculty of Industrial Sciences and Technology, Universiti Malaysia Pahang Al-Sultan Abdullah, Lebuhraya Persiaran Tun Khalil Yaakob, Gambang, Kuantan, Pahang, Malaysia.
Mol Cell Biochem
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Peking University Third Hospital, Beijing, China.
Cardiovascular-Kidney-Metabolic (CKM) syndrome, a newly defined systemic disorder, is characterized by the pathological interplay among diabetes, chronic kidney disease (CKD), and cardiovascular disease (CVD). Recent studies have identified chronic inflammation not only as a central mediator in the pathological progression of CKM syndrome but also as a pivotal molecular hub that drives coordinated damage across multiple organ systems. Mechanistic investigations have revealed that aberrant activation of signaling pathways such as NF-κB, Wnt, PI3K-AKT, JAK-STAT, and PPAR constitutes a complex inflammatory regulatory network.
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