Mechanism of active ingredient compatibility of Dimocarpus longan Lour. leaves in improving glucose and lipid metabolism disorders in type 2 diabetic mellitus rats
- VernacularTitle:龙眼叶活性成分配伍改善2型糖尿病大鼠糖脂代谢紊乱的机制
- Author:
Yanli LIANG
1
;
Shijia AN
1
;
Fengsheng LI
1
;
Jiani MAI
1
;
Anqi HUO
2
;
Jiali WEI
2
;
Zejuan ZHANG
2
;
Shuyan QIN
2
;
Wenqing HUANG
2
;
Jie LIANG
3
Author Information
1. College of Pharmacy，Guangxi University of Chinese Medicine，Nanning 530200，China;Guangxi Key Laboratory of Zhuang and Yao Ethnic Medicine，Nanning 530200，China;Collaborative Innovation Center of Zhuang and Yao Ethnic Medicine，Nanning 530200，China;Guangxi Engineering Research Center of Ethnic Medicine Resources and Application，Nanning 530200，China;Key Δ 基金项目 国家自然科学基金项目（No.82160771）
2. College of Pharmacy，Guangxi University of Chinese Medicine，Nanning 530200，China;Guangxi Key Laboratory of Zhuang and Yao Ethnic Medicine，Nanning 530200，China;Key Δ 基金项目 国家自然科学基金项目（No.82160771）
3. College of Pharmacy，Guangxi University of Chinese Medicine，Nanning 530200，China;Guangxi Key Laboratory of Zhuang and Yao Ethnic Medicine，Nanning 530200，China;Collaborative Innovation Center of Zhuang and Yao Ethnic Medicine，Nanning 530200，China;Guangxi Engineering Research Center of Ethnic Medicine Resources and Application，Nanning 530200，China
- Publication Type:Journal Article
- Keywords:
type 2 diabetes mellitus;
Dimocarpus longan Lour. leaves;
active ingredient compatibility;
quercetin;
quercitrin;
kaempferol;
PI3K/Akt signaling pathway
- From:
China Pharmacy
2026;37(13):1697-1703
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To explore the mechanism of the active ingredient compatibility（quercetin， quercitrin and kaempferol at a mass ratio of 2∶9∶3）of Dimocarpus longan Lour. leaves（abbreviated as CDL） on ameliorating glucose and lipid metabolism disorders in type 2 diabetes mellitus （T2DM） rats. METHODS SD rats were randomly divided into blank control group， model group， metformin hydrochloride group （100 mg/kg）， and CDL high-， medium- and low-dose groups （280， 140， 75 mg/kg）， with 10 rats in each group. Rats in the blank control group were fed with standard chow， while rats in the other groups were given high-sugar and high-fat diet combined with intraperitoneal injection of streptozotocin to establish the T2DM rat model. After successful modeling， rats in each administration group were given corresponding drug solution， and rats in the blank control group and model group were intragastrically administered with equal volume of pure water， once a day， for consecutive 4 weeks. Fasting blood glucose （FBG） was detected at fixed time every week. The curves of oral glucose tolerance test （OGTT） and intraperitoneal insulin tolerance test （IPITT） were plotted， and the area under curve （AUC） was calculated. The pancreatic islet function indexes [fasting insulin （FINS）， homeostasis model assessment of insulin resistance （HOMA-IR）， insulin sensitivity index （ISI）]，blood lipid indexes [total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）] and hepatic glycogen content were determined. The pathological morphological changes of liver and pancreatic tissues were observed. The protein and mRNA expression levels of molecules related to phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway in liver tissues were detected. RESULTS Compared with the blank control group， the FBG， AUC of IPITT curve， AUC of OGTT curve， HOMA-IR， the levels of FINS， TC， TG and LDL-C， as well as the protein and mRNA expression of phosphatase and tensin homolog， forkhead box protein O1 and glycogen synthase kinase-3β in liver tissues were significantly increased in the model group （ P ＜0.05）. ISI， the levels of HDL-C and hepatic glycogen content， along with the protein and mRNA expression of PI3K， insulin receptor substrate-1， Akt and protein expression of phosphorylated Akt in liver tissues were markedly decreased （ P ＜0.05）. In model group rats， the arrangement of hepatocytes was irregular， the overall structure of pancreatic lobules was disordered， and a large number of inflammatory cell infiltration was observed. Compared with the model group， most of the above quantitative indexes were significantly reversed in the CDL high-dose group （ P ＜0.05）， and the pathological lesions of liver and pancreas were obviously alleviated. CONCLUSIONS CDL can regulate glucose and lipid metabolism disorders， elevate insulin sensitivity and relieve insulin resistance in T2DM rats. Its mechanism may be related to the activation of the PI3K/Akt signaling pathway.
