{"title":"富含表没食子儿茶素没食子酸酯的成分通过灭活 Caspase-3/JNK 信号通路减轻组胺诱导的大鼠神经毒性","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":"{\"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}","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
摘要
摄入大量组胺(HIS)会对生物系统产生危险影响。绿茶中最常见的活性儿茶素是表没食子儿茶素没食子酸酯,它具有很强的抗氧化性。我们的研究旨在探讨富含表没食子儿茶素没食子酸酯(EGCGR)对 HIS 引起的神经毒性可能具有的神经保护作用。我们使用了六组雄性大鼠(n = 5),具体如下:(1)蒸馏水;(2&3)EGCGR(分别为100-200毫克/千克体重/天);(4)HIS(1750毫克/千克体重/周);(5&6)HIS + EGCGR。连续 14 天服用 HIS 会诱发严重的神经行为变化,包括抑郁、不协调和空间记忆丧失。广泛的神经元变性和弥漫性胶质增生是观察到的主要组织病理学病变,并通过 casp-3、Cox-2 和 GFAP 的强免疫染色得到证实。此外,与对照组相比,HIS 组的 MDA 水平明显升高,CAT 和 GSH 活性降低。此外,HIS 还能促进细胞凋亡,表现为 JNK 和 Bax 基因表达增加,Bcl-2 基因表达减少。此外,口服 EGCGR 与 HIS 可改善 HIS 诱导的所有神经毒理学参数。我们得出的结论是,HIS可通过破坏氧化剂和抗氧化剂之间的平衡来引起神经中毒,而抗氧化剂可通过调节JNK信号通路来触发细胞凋亡。此外,EGCGR还具有直接或间接的抗组胺作用。
Epigallocatechin gallate-rich fraction alleviates histamine-induced neurotoxicity in rats via inactivating caspase-3/JNK signaling pathways
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.