Objective To evaluate the effect of the phenolic compound naringenin on thermal burn-induced inflammatory responses and oxidative stress in rats. Methods First degree thermal burn injuries were induced in shaved rats by 10 s immersion of the back surface in water at 90℃. Naringenin treatment (25, 50 and 100 mg/kg/day) was initiated 24 h following burn injury, and continued for 7 days. On treatment day 7, serum tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, nitric oxide (NO), prostaglandin (PG)E, caspase-3, leukotriene (LT)-B4 and nuclear factor (NF)-κB levels were quantified. Skin sample glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) levels, and catalase, superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione peroxidase (GPx) activities, were also measured. Results Serum inflammatory biomarkers were significantly increased in thermal-burn injured rats versus uninjured controls. Naringenin significantly inhibited the increased proinflammatory markers at day 7 of treatment. Increased TBARS levels and decreased GSH levels in wounded skin were significantly restored by naringenin treatment at day 7. SOD, catalase, GPx and GST activities were markedly inhibited in wounded skin tissues, and were significantly increased in naringenin-treated rats. Conclusion Naringenin treatment showed anti-inflammatory and antioxidant effects in rats with thermal burn-induced injury.
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http://dx.doi.org/10.1177/0300060517692483 | DOI Listing |
Nutrients
January 2025
Department of Nutrition, School of Public Health, Sun Yat-sen University, 74 Zhong Shan Road 2, Guangzhou 510080, China.
Background: Evidence regarding the individual and combined impact of dietary flavonoids on the risk of metabolic dysfunction associated with steatotic liver disease (MASLD) remains scarce. Our objective is to evaluate the association between individual and multiple dietary flavonoids with MASLD in adults.
Methods: Data sets were obtained from the National Health and Nutrition Examination Survey (NHANES), 2017-2018.
Metabolites
January 2025
Laboratory of Bioresources, Biotechnologies, Ethnopharmacology and Health, Faculty of Sciences, University Mohammed First, Oujda 60000, Morocco.
Background/objectives: Hyperlipidemia is a serious risk factor for cardiovascular diseases and liver steatosis. In this work, we explored the effect of an herbal formula (CBF) containing immature pods and extracts on lipid metabolism disorders and lipoprotein-rich plasma (LRP) oxidation in mice.
Methods: The phenolic composition was determined using HPLC-DAD analysis.
J Med Microbiol
January 2025
Medical Mycology Laboratory, Department of Clinical Analysis and Biomedicine, State University of Maring, Colombo Avenue, 5790, Maring, PR, Brazil.
Fungal infections caused by yeast have increased in recent decades, becoming a major threat to public health. Antifungal therapy represents a challenging problem because, in addition to presenting many side effects, fungal resistance has been increasing in recent years. As a result, the search for new therapeutic agents has advanced with the use of new technologies such as nanoparticles (NPs).
View Article and Find Full Text PDFJ Bone Oncol
February 2025
Liaoning Provincial People's Hospital, Shenyang, Liaoning, China.
Osteosarcoma is a common malignant tumor found in adolescents, characterized by a high metastatic potential and poor prognosis, but it is sensitive to radiotherapy and chemotherapy. Ferroptosis is a novel form of regulated cell death induced by excessive iron accumulation, leading to lipid peroxidation that results in cellular dysfunction and death. Naringenin is a flavonoid known for its anti-cancer properties, yet its role in osteosarcoma has not been thoroughly studied.
View Article and Find Full Text PDFPLoS One
January 2025
Laboratory of Analytical and Molecular Chemistry, Faculty of Sciences Ben M'Sik, Hassan II University of Casablanca, Casablanca, Morocco.
Alzheimer's disease is a neurodegenerative disorder that impairs neurocognitive functions. Acetylcholinesterase, Butyrylcholinesterase, Monoamine Oxidase B, Beta-Secretase, and Glycogen Synthase Kinase Beta play central roles in its pathogenesis. Current medications primarily inhibit AChE but fail to halt or reverse disease progression due to the multifactorial nature of Alzheimer's.
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