{"title":"Epigallocatechin gallate-rich fraction alleviates histamine-induced neurotoxicity in rats via inactivating caspase-3/JNK signaling pathways","authors":"","doi":"10.1016/j.fct.2024.115021","DOIUrl":null,"url":null,"abstract":"<div><div>Ingestion of prominent levels of histamine (HIS) leads to dangerous effects on biological systems. The most frequent and active catechin in green tea is epigallocatechin gallate which has strong antioxidant properties. Our research intended to investigate the possible neuroprotective effect of epigallocatechin gallate-rich fraction (EGCGR) against HIS-inducing neurotoxicity. Six groups of male rats (n = 5) were used as follows: (1) Distilled water, (2&3) EGCGR (100–200 mg/kg BWT/day, respectively), (4) HIS (1750 mg/kg BWT/week, (5&6) HIS + EGCGR. Administration of HIS for 14 days induced severe neurobehavioral changes including depression, incoordination, and loss of spatial memory. Extensive neuronal degeneration with diffuse gliosis was the prominent histopathological lesion observed and confirmed by strong immunostaining of casp-3, Cox-2, and GFAP. Additionally, the HIS group showed a significantly higher MDA level with lower CAT and GSH activity than the control group. Moreover, HIS promoted apoptosis, which is indicated by increasing JNK, and Bax and decreasing Bcl-2 gene expressions. Otherwise, the oral intake of EGCGR with HIS improved all neurotoxicological parameters induced by HIS. We concluded that HIS could cause neurotoxicity via an upset of the equilibrium between oxidants and antioxidants which trigger apoptosis through modulation of JNK signaling pathway. Furthermore, EGCGR has either direct or indirect antihistaminic effects.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":null,"pages":null},"PeriodicalIF":3.9000,"publicationDate":"2024-09-23","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/S0278691524005878","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"FOOD SCIENCE & TECHNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Ingestion of prominent levels of histamine (HIS) leads to dangerous effects on biological systems. The most frequent and active catechin in green tea is epigallocatechin gallate which has strong antioxidant properties. Our research intended to investigate the possible neuroprotective effect of epigallocatechin gallate-rich fraction (EGCGR) against HIS-inducing neurotoxicity. Six groups of male rats (n = 5) were used as follows: (1) Distilled water, (2&3) EGCGR (100–200 mg/kg BWT/day, respectively), (4) HIS (1750 mg/kg BWT/week, (5&6) HIS + EGCGR. Administration of HIS for 14 days induced severe neurobehavioral changes including depression, incoordination, and loss of spatial memory. Extensive neuronal degeneration with diffuse gliosis was the prominent histopathological lesion observed and confirmed by strong immunostaining of casp-3, Cox-2, and GFAP. Additionally, the HIS group showed a significantly higher MDA level with lower CAT and GSH activity than the control group. Moreover, HIS promoted apoptosis, which is indicated by increasing JNK, and Bax and decreasing Bcl-2 gene expressions. Otherwise, the oral intake of EGCGR with HIS improved all neurotoxicological parameters induced by HIS. We concluded that HIS could cause neurotoxicity via an upset of the equilibrium between oxidants and antioxidants which trigger apoptosis through modulation of JNK signaling pathway. Furthermore, EGCGR has either direct or indirect antihistaminic effects.
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.
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