Manal Ismaeil Khalil, Ali Louei Monfared, Hussein Bashar Mahmood
{"title":"辅酶Q10治疗2型糖尿病的生化、组织学和免疫组织化学研究","authors":"Manal Ismaeil Khalil, Ali Louei Monfared, Hussein Bashar Mahmood","doi":"10.4103/RPS.RPS_74_24","DOIUrl":null,"url":null,"abstract":"<p><strong>Background and purpose: </strong>Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by β-cell dysfunction, insulin resistance, and elevated blood sugar levels. Several studies have explored the therapeutic potential of coenzyme Q<sub>10</sub> (CoQ<sub>10</sub>) in managing diabetes, but no reports have examined the possible mechanism of CoQ<sub>10</sub> in T2DM. Here, we reported that CoQ<sub>10</sub> protects pancreatic β-cell structure and function by modulating the expression of mir-33a/mir-21/SREBP1 and described more detailed tissue alterations.</p><p><strong>Experimental approach: </strong>The study randomly divided rats into three groups (n = 10): control, diabetic, and diabetic + CoQ<sub>10</sub>. The diabetic + CoQ<sub>10</sub> group consisted of diabetic rats that were concurrently administered CoQ<sub>10</sub> (20 mg/kg/i.p.) three days/week for eight weeks. In addition to microscopic examination, the study involved evaluating glucose, insulin, and oxidative profiles in the serum and analyzing the levels of cholesterol, mir-33a, mir-2i, and SREBP1 in pancreatic tissue.</p><p><strong>Findings/results: </strong>Our results revealed that CoQ<sub>10</sub> restores glucose/insulin homeostasis, oxidative parameters, cholesterol levels, and the expressions of mir-33a, mir-21, and SREBP1. In addition, the CoQ<sub>10</sub>-treated diabetic rats showed increased active β-cells compared to the diabetic group. The immunohistochemical examination of insulin revealed a higher quantity and larger size of pancreatic islets in the experimental group.</p><p><strong>Conclusion and implications: </strong>The restoration of <i>β</i>-cell integrity following treatment with CoQ<sub>10</sub> may elucidate the therapeutic benefits of this compound in diabetes management, potentially through its influence on the pancreatic expression of mir-33a/mir-21/SREBP1, subsequently maintaining healthy tissue.</p>","PeriodicalId":21075,"journal":{"name":"Research in Pharmaceutical Sciences","volume":"20 2","pages":"292-303"},"PeriodicalIF":2.1000,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118775/pdf/","citationCount":"0","resultStr":"{\"title\":\"Biochemical, histological, and immunohistochemical study on the therapeutic effects and mechanism of coenzyme Q<sub>10</sub> in type 2 diabetes mellitus.\",\"authors\":\"Manal Ismaeil Khalil, Ali Louei Monfared, Hussein Bashar Mahmood\",\"doi\":\"10.4103/RPS.RPS_74_24\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background and purpose: </strong>Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by β-cell dysfunction, insulin resistance, and elevated blood sugar levels. Several studies have explored the therapeutic potential of coenzyme Q<sub>10</sub> (CoQ<sub>10</sub>) in managing diabetes, but no reports have examined the possible mechanism of CoQ<sub>10</sub> in T2DM. Here, we reported that CoQ<sub>10</sub> protects pancreatic β-cell structure and function by modulating the expression of mir-33a/mir-21/SREBP1 and described more detailed tissue alterations.</p><p><strong>Experimental approach: </strong>The study randomly divided rats into three groups (n = 10): control, diabetic, and diabetic + CoQ<sub>10</sub>. The diabetic + CoQ<sub>10</sub> group consisted of diabetic rats that were concurrently administered CoQ<sub>10</sub> (20 mg/kg/i.p.) three days/week for eight weeks. In addition to microscopic examination, the study involved evaluating glucose, insulin, and oxidative profiles in the serum and analyzing the levels of cholesterol, mir-33a, mir-2i, and SREBP1 in pancreatic tissue.</p><p><strong>Findings/results: </strong>Our results revealed that CoQ<sub>10</sub> restores glucose/insulin homeostasis, oxidative parameters, cholesterol levels, and the expressions of mir-33a, mir-21, and SREBP1. In addition, the CoQ<sub>10</sub>-treated diabetic rats showed increased active β-cells compared to the diabetic group. The immunohistochemical examination of insulin revealed a higher quantity and larger size of pancreatic islets in the experimental group.</p><p><strong>Conclusion and implications: </strong>The restoration of <i>β</i>-cell integrity following treatment with CoQ<sub>10</sub> may elucidate the therapeutic benefits of this compound in diabetes management, potentially through its influence on the pancreatic expression of mir-33a/mir-21/SREBP1, subsequently maintaining healthy tissue.</p>\",\"PeriodicalId\":21075,\"journal\":{\"name\":\"Research in Pharmaceutical Sciences\",\"volume\":\"20 2\",\"pages\":\"292-303\"},\"PeriodicalIF\":2.1000,\"publicationDate\":\"2025-03-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118775/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Research in Pharmaceutical Sciences\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4103/RPS.RPS_74_24\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/4/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"CHEMISTRY, MEDICINAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Research in Pharmaceutical Sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4103/RPS.RPS_74_24","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"CHEMISTRY, MEDICINAL","Score":null,"Total":0}
Biochemical, histological, and immunohistochemical study on the therapeutic effects and mechanism of coenzyme Q10 in type 2 diabetes mellitus.
Background and purpose: Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by β-cell dysfunction, insulin resistance, and elevated blood sugar levels. Several studies have explored the therapeutic potential of coenzyme Q10 (CoQ10) in managing diabetes, but no reports have examined the possible mechanism of CoQ10 in T2DM. Here, we reported that CoQ10 protects pancreatic β-cell structure and function by modulating the expression of mir-33a/mir-21/SREBP1 and described more detailed tissue alterations.
Experimental approach: The study randomly divided rats into three groups (n = 10): control, diabetic, and diabetic + CoQ10. The diabetic + CoQ10 group consisted of diabetic rats that were concurrently administered CoQ10 (20 mg/kg/i.p.) three days/week for eight weeks. In addition to microscopic examination, the study involved evaluating glucose, insulin, and oxidative profiles in the serum and analyzing the levels of cholesterol, mir-33a, mir-2i, and SREBP1 in pancreatic tissue.
Findings/results: Our results revealed that CoQ10 restores glucose/insulin homeostasis, oxidative parameters, cholesterol levels, and the expressions of mir-33a, mir-21, and SREBP1. In addition, the CoQ10-treated diabetic rats showed increased active β-cells compared to the diabetic group. The immunohistochemical examination of insulin revealed a higher quantity and larger size of pancreatic islets in the experimental group.
Conclusion and implications: The restoration of β-cell integrity following treatment with CoQ10 may elucidate the therapeutic benefits of this compound in diabetes management, potentially through its influence on the pancreatic expression of mir-33a/mir-21/SREBP1, subsequently maintaining healthy tissue.
期刊介绍:
Research in Pharmaceutical Sciences (RPS) is included in Thomson Reuters ESCI Web of Science (searchable at WoS master journal list), indexed with PubMed and PubMed Central and abstracted in the Elsevier Bibliographic Databases. Databases include Scopus, EMBASE, EMCare, EMBiology and Elsevier BIOBASE. It is also indexed in several specialized databases including Scientific Information Database (SID), Google Scholar, Iran Medex, Magiran, Index Copernicus (IC) and Islamic World Science Citation Center (ISC).