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1.
Acta Biochim Biophys Sin (Shanghai) ; 50(3): 298-306, 2018 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-29425256

RESUMO

Type 2 diabetes mellitus (T2DM) leads to cognitive impairment (CI), but there have been no effective pharmacotherapies or drugs for cognitive dysfunction in T2DM. Dihydromyricetin (DHM) is a natural flavonoid compound extracted from the leaves of Ampelopsis grossedentata and has various pharmacological effects including anti-oxidant and anti-diabetes. Thus, we investigated the effects of DHM on CI in T2DM mouse model and its possible mechanism. To induce T2DM, mice were fed with high-sugar and high-fat diet for 8 weeks, followed by a low dose streptozotocin (STZ) administration. After the successful induction of T2DM mouse model, mice were treated respectively with equal volume of saline (T2DM group), 125 mg/kg/d DHM (L-DHM group), or 250 mg/kg/d DHM (H-DHM group). After 16 weeks of DHM administration, the body weight (BW), fasting blood glucose, blood lipids, intraperitoneal glucose tolerance (IPGT), and cognitive function were determined. Then, alterations in the expressions of oxidative stress markers and brain-derived neurotrophic factor (BDNF) in the hippocampus were investigated. Our findings demonstrated that DHM could significantly ameliorate CI and reverse aberrant glucose and lipid metabolism in T2DM mice, likely through the suppression of oxidative stress and enhancement of BDNF-mediated neuroprotection. In conclusion, our results suggest that DHM is a promising candidate for the treatment of T2DM-induced cognitive dysfunction.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Disfunção Cognitiva/prevenção & controle , Diabetes Mellitus Tipo 2/complicações , Flavonóis/farmacologia , Neuroproteção/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Ampelopsis/química , Animais , Glicemia/metabolismo , Fator Neurotrófico Derivado do Encéfalo/genética , Disfunção Cognitiva/etiologia , Disfunção Cognitiva/metabolismo , Diabetes Mellitus Experimental/sangue , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Tipo 2/sangue , Aprendizagem em Labirinto/efeitos dos fármacos , Camundongos , Fármacos Neuroprotetores/farmacologia , Fitoterapia , Extratos Vegetais/farmacologia
2.
Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 33(6): 568-571, 2017 Jun 08.
Artigo em Chinês | MEDLINE | ID: mdl-29931910

RESUMO

OBJECTIVE: To observe the effects of lyceum barbarum polysaccharide (LBP) on insulin resistance of HepG2 cells and investigate its possible mechanism. METHODS: IR-HepG2 cell model was induced with high glucose and high insulin in combination for 24 hours,with 104/vaccination in the 96-well plates, hole density after adherent cells (30 µg/ml、100 µg/ml、300 µg/ml) LBP cultivate 48 h, 200 µl/hole, each all had four holes. The effects of LBP at different concentrations on HepG2 cell activity and insulin resistance were tested. Intracellular malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were detected. The expressions of related proteins in insulin signal transduction pathways such as insulin receptor substrate-2(IRS-2), phosphatidylinositol-3-kinase(PI3-K), protein kinase B(Akt) and glucose transport-2(GLUT2) were determined. RESULTS: Compared with normal control group, the content of MDA was increased significantly and the activity of SOD and the expression levels of IRS-2,PI-3K,Akt and GLUT2 were decreased significantly in the IR model group. Compared with IR model group, medium and high concentrations of LBP decreased the content of MDA and increased the activity of SOD and the expression levels of IRS-2, PI-3K, Akt and GLUT2 in insulin-resistant HepG2 cells. MTT showed that at the same time, the OD value gradually decreased with the increase of LBP's concentration; under the same concentration of LBP, the OD value also gradually decreased with the extension of time, which indicated that LBP inhibited the proliferation of HepG2 cells with time and concentration-dependent manner. Glucose consumption experiment indicated that medium and high concentration of LBP could increase the glucose consumption of insulin-resistant HepG2 cells significantly, but low concentration of LBP had no significant impacted on glucose consumption of insulin-resistant HepG2 cells. CONCLUSIONS: Medium and high concentration of LBP can improve insulin resistance of HepG2 cell, its mechanisns may be associated with decreasing the level of oxidative stress and increasing the protein expressions of insulin signaling pathway.


Assuntos
Medicamentos de Ervas Chinesas/farmacologia , Resistência à Insulina , Transdução de Sinais/efeitos dos fármacos , Glucose , Transportador de Glucose Tipo 2/metabolismo , Células Hep G2 , Humanos , Insulina , Proteínas Substratos do Receptor de Insulina/metabolismo , Estresse Oxidativo , Fosfatidilinositol 3-Quinases/metabolismo , Polissacarídeos , Proteínas Proto-Oncogênicas c-akt/metabolismo
3.
Acta Pharmacol Sin ; 33(8): 1023-9, 2012 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-22820911

RESUMO

AIM: To investigate the effect of arecoline, a major component of betel nut, on vascular endothelial function in high fructose-fed rats and the potential mechanisms underlying the effect. METHODS: Male Wistar rats were fed a high-fructose or control diet for 16 weeks. At the beginning of week 13, the rats were injected ip with low (0.5 mg·kg(-1)·d(-1)), medium (1.0 mg·kg(-1)·d(-1)) or high (5.0 mg·kg(-1)·d(-1)) doses of arecoline for 4 weeks. At the termination of the treatments, blood was collected, fasting blood glucose (FBG) and serum insulin (FSI) levels were measured, and insulin sensitivity index (ISI) was calculated. The thoracic aortas were isolated and aortic rings were prepared for studying ACh-induced endothelium-dependent vasorelaxation (EDVR). The mRNA and protein expression of cystathionine-γ-lyase (CSE) in the thoracic aortas was analyzed using RT-PCR and Western blot analysis, respectively. RESULTS: In high fructose-fed rats, the levels of FBG and FSI were remarkably increased, whereas the ISI and the mRNA and protein expression of CSE were significantly decreased. ACh-induced EDVR in the aortic rings from high fructose-fed rats was remarkably reduced. These changes were reversed by treatment with high dose arecoline. Pretreatment of the aortic rings rings from high fructose-fed rats with the CSE inhibitor propargylglycine (10 mmol/L) or the ATP-sensitive potassium (K(ATP)) channel blocker glibenclamide (10 mmol/L) abolished the restoration of ACh-induced EDVR by high dose arecoline. On the contrary, treatment with high dose arecoline significantly impaired ACh-induced EDVR in the aortic rings from control rats, and pretreatment with propargylglycine or glibenclamide did not cause further changes. CONCLUSION: Arecoline treatment improves ACh-induced EDVR in high fructose-fed rats, and the potential mechanism of action might be associated with increase of CSE expression and activation of K(ATP) channels by arecoline.


Assuntos
Arecolina/farmacologia , Cistationina gama-Liase/biossíntese , Endotélio Vascular/efeitos dos fármacos , Endotélio Vascular/enzimologia , Frutose/toxicidade , Canais KATP/metabolismo , Animais , Aorta Torácica/efeitos dos fármacos , Aorta Torácica/enzimologia , Relação Dose-Resposta a Droga , Endotélio Vascular/fisiologia , Frutose/administração & dosagem , Regulação Enzimológica da Expressão Gênica , Masculino , Técnicas de Cultura de Órgãos , Ratos , Ratos Wistar
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