{"title":"地奥司明对毒死蜱诱导的脑损伤的神经保护作用是通过调节 PPAR-γ 和 NF-κB/AP-1 信号介导的。","authors":"","doi":"10.1016/j.fct.2024.114967","DOIUrl":null,"url":null,"abstract":"<div><p>Chlorpyrifos (CPF) is a widely used organophosphate (OP) pesticide. Unfortunately, pesticides are known to cause neuronal intoxication. Diosmin (DS) is an antioxidant, anti-inflammatory, and neuroprotective flavonoid with high efficacy and safety. We plan to investigate the efficacy of DS in treating CPF-induced neurotoxicity, as well as the mechanisms underlying the protective effects. In our study, rats were randomized into 5 groups: control, DS (50 mg/kg), CPF (10 mg/kg), CPF + DS (25 mg/kg), and CPF + DS (50 mg/kg). The results indicated that DS ameliorated neuronal intoxication induced by CPF, evidenced by decreasing Tau, p-Tau, and β-amyloid. Histological examinations support these findings. DS significantly ameliorated CPF-induced neuronal oxidative injury by decreasing MDA content and elevating GSH, GST, and SOD levels mediated by PPAR-γ upregulation. DS suppressed CPF-induced brain inflammation by decreasing MPO enzymatic activity and TNF-α, IL-1β, and IL-6 levels mediated by downregulation of NF-κB/AP-1(c-FOS and c-JUN) signal. Of note, DS protective effects were dose dependent. In conclusion, our data suggested that DS was a promising therapeutic strategy for attenuating CPF-induced neuronal intoxication by restoring oxidant-antioxidant balance and inhibiting inflammatory response in brain tissues.</p></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":null,"pages":null},"PeriodicalIF":3.9000,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Neuroprotective effect of diosmin against chlorpyrifos-induced brain intoxication was mediated by regulating PPAR-γ and NF-κB/AP-1 signals\",\"authors\":\"\",\"doi\":\"10.1016/j.fct.2024.114967\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Chlorpyrifos (CPF) is a widely used organophosphate (OP) pesticide. Unfortunately, pesticides are known to cause neuronal intoxication. Diosmin (DS) is an antioxidant, anti-inflammatory, and neuroprotective flavonoid with high efficacy and safety. We plan to investigate the efficacy of DS in treating CPF-induced neurotoxicity, as well as the mechanisms underlying the protective effects. In our study, rats were randomized into 5 groups: control, DS (50 mg/kg), CPF (10 mg/kg), CPF + DS (25 mg/kg), and CPF + DS (50 mg/kg). The results indicated that DS ameliorated neuronal intoxication induced by CPF, evidenced by decreasing Tau, p-Tau, and β-amyloid. Histological examinations support these findings. DS significantly ameliorated CPF-induced neuronal oxidative injury by decreasing MDA content and elevating GSH, GST, and SOD levels mediated by PPAR-γ upregulation. DS suppressed CPF-induced brain inflammation by decreasing MPO enzymatic activity and TNF-α, IL-1β, and IL-6 levels mediated by downregulation of NF-κB/AP-1(c-FOS and c-JUN) signal. Of note, DS protective effects were dose dependent. In conclusion, our data suggested that DS was a promising therapeutic strategy for attenuating CPF-induced neuronal intoxication by restoring oxidant-antioxidant balance and inhibiting inflammatory response in brain tissues.</p></div>\",\"PeriodicalId\":317,\"journal\":{\"name\":\"Food and Chemical Toxicology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2024-08-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Food and Chemical Toxicology\",\"FirstCategoryId\":\"97\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0278691524005337\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"FOOD SCIENCE & TECHNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Food and Chemical Toxicology","FirstCategoryId":"97","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0278691524005337","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"FOOD SCIENCE & TECHNOLOGY","Score":null,"Total":0}
Neuroprotective effect of diosmin against chlorpyrifos-induced brain intoxication was mediated by regulating PPAR-γ and NF-κB/AP-1 signals
Chlorpyrifos (CPF) is a widely used organophosphate (OP) pesticide. Unfortunately, pesticides are known to cause neuronal intoxication. Diosmin (DS) is an antioxidant, anti-inflammatory, and neuroprotective flavonoid with high efficacy and safety. We plan to investigate the efficacy of DS in treating CPF-induced neurotoxicity, as well as the mechanisms underlying the protective effects. In our study, rats were randomized into 5 groups: control, DS (50 mg/kg), CPF (10 mg/kg), CPF + DS (25 mg/kg), and CPF + DS (50 mg/kg). The results indicated that DS ameliorated neuronal intoxication induced by CPF, evidenced by decreasing Tau, p-Tau, and β-amyloid. Histological examinations support these findings. DS significantly ameliorated CPF-induced neuronal oxidative injury by decreasing MDA content and elevating GSH, GST, and SOD levels mediated by PPAR-γ upregulation. DS suppressed CPF-induced brain inflammation by decreasing MPO enzymatic activity and TNF-α, IL-1β, and IL-6 levels mediated by downregulation of NF-κB/AP-1(c-FOS and c-JUN) signal. Of note, DS protective effects were dose dependent. In conclusion, our data suggested that DS was a promising therapeutic strategy for attenuating CPF-induced neuronal intoxication by restoring oxidant-antioxidant balance and inhibiting inflammatory response in brain tissues.
期刊介绍:
Food and Chemical Toxicology (FCT), an internationally renowned journal, that publishes original research articles and reviews on toxic effects, in animals and humans, of natural or synthetic chemicals occurring in the human environment with particular emphasis on food, drugs, and chemicals, including agricultural and industrial safety, and consumer product safety. Areas such as safety evaluation of novel foods and ingredients, biotechnologically-derived products, and nanomaterials are included in the scope of the journal. FCT also encourages submission of papers on inter-relationships between nutrition and toxicology and on in vitro techniques, particularly those fostering the 3 Rs.
The principal aim of the journal is to publish high impact, scholarly work and to serve as a multidisciplinary forum for research in toxicology. Papers submitted will be judged on the basis of scientific originality and contribution to the field, quality and subject matter. Studies should address at least one of the following:
-Adverse physiological/biochemical, or pathological changes induced by specific defined substances
-New techniques for assessing potential toxicity, including molecular biology
-Mechanisms underlying toxic phenomena
-Toxicological examinations of specific chemicals or consumer products, both those showing adverse effects and those demonstrating safety, that meet current standards of scientific acceptability.
Authors must clearly and briefly identify what novel toxic effect (s) or toxic mechanism (s) of the chemical are being reported and what their significance is in the abstract. Furthermore, sufficient doses should be included in order to provide information on NOAEL/LOAEL values.