补充冻干草本山柰能有效调节糖尿病 BALB/c 小鼠因高血糖引起的氧化应激和细胞凋亡

IF 3.4 Q2 PHARMACOLOGY & PHARMACY
Flavius Phrangsngi Nonglang, Revelbornstar Snaitang, Dhritiman Roy, Surya Bhan
{"title":"补充冻干草本山柰能有效调节糖尿病 BALB/c 小鼠因高血糖引起的氧化应激和细胞凋亡","authors":"Flavius Phrangsngi Nonglang,&nbsp;Revelbornstar Snaitang,&nbsp;Dhritiman Roy,&nbsp;Surya Bhan","doi":"10.1186/s43094-025-00772-z","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>A dysfunction in insulin secretion or action leads to hyperglycemia. Hyperglycemia then causes the activation of pathways that result in increased production of reactive oxygen and nitrogen species (ROS/RNS) levels, ultimately causing oxidative stress. Oxidative stress overload then causes cellular damage and also promotes the increased activation of the apoptosis pathway inducing cell death. Thus, regulation of glucose homeostasis to prevent hyperglycemia is crucial. In this study, the potential protective effect of <i>Kaempferia galanga</i> herbal extract (KGE) on hyperglycemia-induced oxidative stress and apoptosis was investigated.</p><h3>Result</h3><p>In this study, <i>Kaempferia galanga</i> (KG) herbal extracts, namely aqueous (KGA), ethanolic (KGE), methanolic (KGM), and chloroform (KGC), were tested for their antioxidant activity. In <i>in vitro</i> antioxidant assays, KG ethanolic extract (KGE) has the highest antioxidant activity out of all the extracts. High-performance thin layer chromatography phytochemical fingerprinting (HPTLC) analysis confirms that the presence of more antioxidant compounds in herbal KGE and ethyl-p methoxy cinnamate (EPMC) was the active phytochemical. Thus, KGE was chosen for <i>in vivo</i> studies. An intraperitoneal streptozotocin (STZ) administration produced a diabetic mouse model. <i>In vivo</i> herbal KGE treatment positively modulates SOD and CAT gene and protein expression in diabetic mice. Tissue protection from herbal KGE supplementation is supported by liver electron microscopy. In diabetic mice, herbal KGE supplementation reduces DNA fragmentation in the liver, kidney, pancreas, and heart by upregulating the gene and protein expression of anti-apoptotic BCL-2, inhibiting BAX expression, and ultimately inhibiting caspase-3 (CAS-3) expression. Herbal KGE supplementation in diabetic mice maintains insulin levels in serum and pancreas, indicating its protective role in preventing pancreatic damage or promoting β cell regeneration. Molecular docking analysis shows EPMC's high binding affinity for CAS-3, BAX, and BCL-2 compared to metformin suggesting that it may be responsible for modulating apoptotic protein expression.</p><h3>Discussion</h3><p>Herbal KGE supplementation protects against diabetes-induced tissue damage and apoptosis by reducing hyperglycemia-induced oxidative stress and apoptosis, and EPMC may be the active component eliciting the effect.</p></div>","PeriodicalId":577,"journal":{"name":"Future Journal of Pharmaceutical Sciences","volume":"11 1","pages":""},"PeriodicalIF":3.4000,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://fjps.springeropen.com/counter/pdf/10.1186/s43094-025-00772-z","citationCount":"0","resultStr":"{\"title\":\"Freeze-dried herbal Kaempferia galanga supplementation effectively modulates hyperglycemia-induced oxidative stress and apoptosis in diabetic BALB/c mice\",\"authors\":\"Flavius Phrangsngi Nonglang,&nbsp;Revelbornstar Snaitang,&nbsp;Dhritiman Roy,&nbsp;Surya Bhan\",\"doi\":\"10.1186/s43094-025-00772-z\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>A dysfunction in insulin secretion or action leads to hyperglycemia. Hyperglycemia then causes the activation of pathways that result in increased production of reactive oxygen and nitrogen species (ROS/RNS) levels, ultimately causing oxidative stress. Oxidative stress overload then causes cellular damage and also promotes the increased activation of the apoptosis pathway inducing cell death. Thus, regulation of glucose homeostasis to prevent hyperglycemia is crucial. In this study, the potential protective effect of <i>Kaempferia galanga</i> herbal extract (KGE) on hyperglycemia-induced oxidative stress and apoptosis was investigated.</p><h3>Result</h3><p>In this study, <i>Kaempferia galanga</i> (KG) herbal extracts, namely aqueous (KGA), ethanolic (KGE), methanolic (KGM), and chloroform (KGC), were tested for their antioxidant activity. In <i>in vitro</i> antioxidant assays, KG ethanolic extract (KGE) has the highest antioxidant activity out of all the extracts. High-performance thin layer chromatography phytochemical fingerprinting (HPTLC) analysis confirms that the presence of more antioxidant compounds in herbal KGE and ethyl-p methoxy cinnamate (EPMC) was the active phytochemical. Thus, KGE was chosen for <i>in vivo</i> studies. An intraperitoneal streptozotocin (STZ) administration produced a diabetic mouse model. <i>In vivo</i> herbal KGE treatment positively modulates SOD and CAT gene and protein expression in diabetic mice. Tissue protection from herbal KGE supplementation is supported by liver electron microscopy. In diabetic mice, herbal KGE supplementation reduces DNA fragmentation in the liver, kidney, pancreas, and heart by upregulating the gene and protein expression of anti-apoptotic BCL-2, inhibiting BAX expression, and ultimately inhibiting caspase-3 (CAS-3) expression. Herbal KGE supplementation in diabetic mice maintains insulin levels in serum and pancreas, indicating its protective role in preventing pancreatic damage or promoting β cell regeneration. Molecular docking analysis shows EPMC's high binding affinity for CAS-3, BAX, and BCL-2 compared to metformin suggesting that it may be responsible for modulating apoptotic protein expression.</p><h3>Discussion</h3><p>Herbal KGE supplementation protects against diabetes-induced tissue damage and apoptosis by reducing hyperglycemia-induced oxidative stress and apoptosis, and EPMC may be the active component eliciting the effect.</p></div>\",\"PeriodicalId\":577,\"journal\":{\"name\":\"Future Journal of Pharmaceutical Sciences\",\"volume\":\"11 1\",\"pages\":\"\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2025-02-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://fjps.springeropen.com/counter/pdf/10.1186/s43094-025-00772-z\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Future Journal of Pharmaceutical Sciences\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://link.springer.com/article/10.1186/s43094-025-00772-z\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PHARMACOLOGY & PHARMACY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Future Journal of Pharmaceutical Sciences","FirstCategoryId":"1085","ListUrlMain":"https://link.springer.com/article/10.1186/s43094-025-00772-z","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0

摘要

背景:胰岛素分泌或作用紊乱可导致高血糖。随后,高血糖会激活导致活性氧和氮(ROS/RNS)水平增加的通路,最终导致氧化应激。氧化应激超载导致细胞损伤,并促进细胞凋亡通路的激活,诱导细胞死亡。因此,调节葡萄糖稳态以防止高血糖是至关重要的。本研究探讨了山柰高良姜提取物(KGE)对高血糖诱导的氧化应激和细胞凋亡的潜在保护作用。结果采用水提液(KGA)、乙醇提液(KGE)、甲醇提液(KGM)和氯仿提液(KGC)对山奈良姜(KG)进行抗氧化活性测定。在体外抗氧化试验中,KG乙醇提取物(KGE)的抗氧化活性最高。高效薄层色谱植物化学指纹图谱(HPTLC)分析证实,中药KGE中含有较多的抗氧化成分,肉桂酸乙酯(EPMC)为活性成分。因此,我们选择KGE进行体内研究。腹腔注射链脲佐菌素(STZ)建立糖尿病小鼠模型。中药KGE对糖尿病小鼠体内SOD、CAT基因及蛋白表达有正向调节作用。肝脏电子显微镜证实了草药KGE补充剂对组织的保护作用。在糖尿病小鼠中,草药KGE补充通过上调抗凋亡BCL-2基因和蛋白表达,抑制BAX表达,最终抑制caspase-3 (CAS-3)表达,减少肝脏、肾脏、胰腺和心脏的DNA片段化。补充KGE可维持糖尿病小鼠血清和胰腺中的胰岛素水平,表明其具有预防胰腺损伤或促进β细胞再生的保护作用。分子对接分析显示,与二甲双胍相比,EPMC对CAS-3、BAX和BCL-2具有较高的结合亲和力,提示EPMC可能参与调节凋亡蛋白的表达。探讨中药KGE通过降低高血糖诱导的氧化应激和细胞凋亡,保护糖尿病诱导的组织损伤和细胞凋亡,EPMC可能是其活性成分。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Freeze-dried herbal Kaempferia galanga supplementation effectively modulates hyperglycemia-induced oxidative stress and apoptosis in diabetic BALB/c mice

Background

A dysfunction in insulin secretion or action leads to hyperglycemia. Hyperglycemia then causes the activation of pathways that result in increased production of reactive oxygen and nitrogen species (ROS/RNS) levels, ultimately causing oxidative stress. Oxidative stress overload then causes cellular damage and also promotes the increased activation of the apoptosis pathway inducing cell death. Thus, regulation of glucose homeostasis to prevent hyperglycemia is crucial. In this study, the potential protective effect of Kaempferia galanga herbal extract (KGE) on hyperglycemia-induced oxidative stress and apoptosis was investigated.

Result

In this study, Kaempferia galanga (KG) herbal extracts, namely aqueous (KGA), ethanolic (KGE), methanolic (KGM), and chloroform (KGC), were tested for their antioxidant activity. In in vitro antioxidant assays, KG ethanolic extract (KGE) has the highest antioxidant activity out of all the extracts. High-performance thin layer chromatography phytochemical fingerprinting (HPTLC) analysis confirms that the presence of more antioxidant compounds in herbal KGE and ethyl-p methoxy cinnamate (EPMC) was the active phytochemical. Thus, KGE was chosen for in vivo studies. An intraperitoneal streptozotocin (STZ) administration produced a diabetic mouse model. In vivo herbal KGE treatment positively modulates SOD and CAT gene and protein expression in diabetic mice. Tissue protection from herbal KGE supplementation is supported by liver electron microscopy. In diabetic mice, herbal KGE supplementation reduces DNA fragmentation in the liver, kidney, pancreas, and heart by upregulating the gene and protein expression of anti-apoptotic BCL-2, inhibiting BAX expression, and ultimately inhibiting caspase-3 (CAS-3) expression. Herbal KGE supplementation in diabetic mice maintains insulin levels in serum and pancreas, indicating its protective role in preventing pancreatic damage or promoting β cell regeneration. Molecular docking analysis shows EPMC's high binding affinity for CAS-3, BAX, and BCL-2 compared to metformin suggesting that it may be responsible for modulating apoptotic protein expression.

Discussion

Herbal KGE supplementation protects against diabetes-induced tissue damage and apoptosis by reducing hyperglycemia-induced oxidative stress and apoptosis, and EPMC may be the active component eliciting the effect.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
44
审稿时长
23 weeks
期刊介绍: Future Journal of Pharmaceutical Sciences (FJPS) is the official journal of the Future University in Egypt. It is a peer-reviewed, open access journal which publishes original research articles, review articles and case studies on all aspects of pharmaceutical sciences and technologies, pharmacy practice and related clinical aspects, and pharmacy education. The journal publishes articles covering developments in drug absorption and metabolism, pharmacokinetics and dynamics, drug delivery systems, drug targeting and nano-technology. It also covers development of new systems, methods and techniques in pharmacy education and practice. The scope of the journal also extends to cover advancements in toxicology, cell and molecular biology, biomedical research, clinical and pharmaceutical microbiology, pharmaceutical biotechnology, medicinal chemistry, phytochemistry and nutraceuticals.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信