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An Optimum Dose of Olive Leaf Extract Improves Insulin Receptor Substrate-1,Tyrosine Kinase,and glucose transporters,While High Doses Have Genotoxic and Apoptotic Effects

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American Journal of Plant Sciences 2019年第11期10卷 1933-1948页

作者： Abdurrahim Kocyigit Burcin Kasap Eray Metin Guler Humeyra Nur Kaleli Mustafa Kesmen Murat Dikilitas Ersin Karatas Department of Medical Biochemistry Medical FacultyBezmialem Vakif UniversityIstanbulTurkey Traditional and Complementary Medicine Advanced Research and Application Center(GETAMER) Bezmialem Vakif UniversityIstanbulTurkey Department of Molecular Biology Geneticsand BioengineeringSabanci UniversityIstanbulTurkey Republic of Turkey Ministry of Agriculture and Forestry Istanbul Pendik Veterinary Control Institute IstanbulTurkey Department of Plant Protection Agricultural FacultyHarran UniversityS.UrfaTurkey 6Department of Molecular Biology and GeneticsGebze Technical UniversityKocaeliTurkey

Type 2 diabetes is the most common type of diabetes. Conventionally many drugs are used for the treatment of diabetes such as biguanides, sulfonylureas, meglitinides, etc. But the desired effective treatment is still not to be achieved. So researches are going on for the development of effective alternative therapy against diabetes. Olive leaves are traditionally used in the treatment of the disease. However, studies on its mechanism of action are not yet enough. The aim of this study was to investigate whether olive leaf extract (OLE) improves insulin receptor substrate-1 (IRS-1), tyrosine kinase (TK), GLUT-2, and GLUT-4. Oleuropein levels were analyzed from OLE obtained by using four different solvents, and the highest content of methanol extract was selected for the study. Different concentrations of OLE (2.5 to 320 μg/mL) were incubated with hepatocellular carcinoma (HepG2) cells for 24 hours. After incubation, cell viability was assessed based on luminometric ATP cell viability assay kit. Intracellular reactive oxygen species (ROS) generating level was detected using 2,7dichlorodihydrofluorescein-diacetate (H2DCF-DA) fluorescent probes. Apoptosis was evaluated by acridine orange/ethidium bromide double staining method. Genotoxicity was evaluated by alkaline single cell gel electrophoresis assay (Comet Assay). Protein expression levels of IRS-1, TK, GLUT-2, and GLUT-4 were analyzed by western blotting technique from the obtained cell lysates. Although an optimum doses of OLE (10 μg/mL) maximally increased cell proliferation, decreased ROS generation improved IRS-1, TK, GLUT-2, and GLUT-4 protein expression levels (about fivefold), higher doses (10 to 320 μg/mL) markedly decreased the cell viability, increased DNA damage, apoptosis and ROS generation in a concentration-dependent manner. OLE can be used in the treatment of type 2 diabetes. However, in order to find the most effective and non-toxic concentration, dose optimization is required.

关键词： Phytotherapy Diabetes Mellitus Olive Leaf Extract glucose transporters Insulin Receptors

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Moderate exercise prevents neurodegeneration in D-galactose-induced aging mice

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Neural Regeneration Research 2016年第5期11卷 807-815页

作者： Li Li Meng Xu Bo Shen Man Li Qian Gao Shou-gang Wei Department of Infectious Medicine Beijing You An Hospital Affiliated to Capital Medical University Department of Children's and Women's Health School of Public Health Capital Medical University

D-galactose has been widely used in aging research because of its efficacy in inducing senescence and accelerating aging in animal models. The present study investigated the benefits of exercise for preventing neurodegeneration, such as synaptic plasticity, spatial learning and memory abilities, in mouse models of aging. D-galactose-induced aging mice were administered daily subcutaneous injections of D-galactose at the base of the neck for 10 consecutive weeks. Then, the mice were subjected to exercise training by running on a treadmill for 6 days a week. Shortened escape latency in a Morris water maze test indicated that exercise improved learning and memory in aging mice. The ameliorative changes were likely induced by an upregulation of Bcl-2 and brain-derived neurotrophic factor, the repression of apoptosis factors such as Fas and Bax, and an increase in the activity of glucose transporters-1 and 4. The data suggest moderate exercise may retard or inhibit neurodegeneration in D-galactose-induced aging mice.

关键词： nerve regeneration D-galactose brain aging behavioral performance brain-derived neurotrophic.factor neuronal apoptosis glucose transporters synaptic plasticity neurodegeneration neural regeneration

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Chronic intermittent hypoxia from pedo-stage decreases glucose transporter 4 expression in adipose tissue and causes insulin resistance

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Chinese Medical Journal 2010年第4期123卷 463-470页

作者： CHEN Lin CAO Zhao-long HAN Fang GAO Zhan-cheng HE Quan-ying Department of Pneumology Peking University People's Hospital Beijing 100044 China

Background The persistence of sleep disordered breathing （SDB） symptoms after tonsil and/or adenoid （T＆A） surgery are common in children with obstructive sleep apnea （OSA）. We tested the hypothesis that disturbances of glucose transporters （GLUTs） in intraabdominal adipose tissue caused by chronic intermittent hypoxia （CIH） from the pedo-period could facilitate the appearance of periphery insulin resistance in Sprague-Dawley （SD） rats. We tested the hypothesis that the changes of GLUTs in adipose tissue may be one of the reasons for persistent SDB among clinical OSA children after T＆A surgery. Methods Thirty 21-day-old SD rats were randomly divided into a CIH group, a chronic continuous hypoxia （CCH） group and a normal oxygen group （control group） and exposed for 40 days. The changes of weight, fasting blood glucose and fasting blood insulin levels were measured. Hyperinsulinemic-euglycemic clamp techniques were used to measure insulin resistance in each animal. Real-time quantitative PCR and Western blotting were used to measure GLUT mRNA and proteins in intraabdominal adipose tissue. Additional intraabdomial white adipose tissue （WAT） was also processed into paraffin sections and directly observed for GLUTs1-4 expression. Results When compared with control group, CIH increased blood fasting insulin levels, （245.07±53.89） pg/ml vs. （168.63±38.70） pg/ml, P=-0.038, and decreased the mean glucose infusion rate （GIR）, （7.25±1.29） mg·kg^-1·min^-1 vs. （13.34±1.54） mg·kg^-1·min^-1, P 〈0.001. GLUT-4 mRNA and protein expression was significantly reduced after CIH compared with CCH or normal oxygen rats, 0.002±0.002 vs. 0.039±0.009, P 〈0.001; 0.642±0.073 vs. 1.000±0.103, P=0.035. Conclusions CIH in young rats could induce insulin resistance via adverse effects on glycometabolism. These findings emphasize the importance of early detection and treatment of insulin insensitivity in obese childhood OSA.

关键词： sleep apnea syndrome insulin resistance glucose transporters hypoxia childhood

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