Effects of total glucosides of paeony on enhancing insulin sensitivity and antagonizing nonalcoholic fatty liver in rats / 中国中药杂志

<p><b>OBJECTIVE</b>To study the pathological changes of blood glucose, serum lipid, insulin resistance, liver function, liver cell denaturalization of total glucosides of paeony on nonalcoholic fatty liver rats caused by insulin resistance and discuss the acting mechanism.</p><p><b>METHOD</b>Adult SD rats were maintained on high-fat-sugar-salt diet for 56 days. In the 57th day, their fasting blood glucose (FBG) and 2-hours blood glucose after oral glucose tolerance test (OGTT-2 hBG) were mensurated, according to which and the weight the rats were divided randomly into nonalcoholic fatty liver model group, metformin group (0.2 g x kg(-1)) and total glucosides of paeony group (high dosage 0.15 g x kg(-1), low dosage 0.05 g x kg(-1)). All the rats were still administered the same diet and given different drugs by intragastric administration for 28 days. In the 29th day, all of them were killed and the blood was sampled to measure the levels of blood glucose [FBG, OGTT-2 hBG, fasting insulin (Fins)] and serum lipid [free fatty acids (FFA), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C)], then the HOMA insulin resistance index (HOMA-IRI, fasting glucosexinsulin) and insulin sensitivity index (ISI) were counted. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), cholinesterase (ChE), superoxide dismutase (SOD) and the contents of malondialdehyde (MDA) were measured also. Livers were weighed and collected to be observed the pathological changes.</p><p><b>RESULT</b>Compared with normal group, in nonalcoholic fatty liver model group the levels of Fins and IRI were increased obviously (P < 0.01), ISI were decreased (P < 0.01), FFA, TG, TC, LDL-C were increased (P < 0.01), HDL-C were decreased (P < 0.05); the content of MDA were increased (P < 0.05), the activities of SOD were decreased (P < 0.01); AST, ALT and ChE were increased (P < 0.05, or P < 0.01), the pathological changes of liver fat were severe (P < 0.01). In glucosides of paeony group and metformin group, hyperinsulinaemia and insulin resistence were resisted (P < 0.05, or P < 0.01); the levels of FFA, TG, TC, LDL-C were decreased and HDL-C were increased (P < 0.05, or P < 0.01); the activities of AST, ALT, ChE were decreased (P < 0.05, or P < 0.01) and SOD were increased (P < 0.01). The contents of MDA were decreased (P < 0.05). The levels of FBG and 2 hBG in metformin group were decreased but in total glucosides of paeony group were not decreased obviously.</p><p><b>CONCLUSION</b>Total glucosides of paeony may protect liver function and modulate serum lipid for the fatty liver rats caused by insulin resistance, and its action mechanism may be concerned with enhancing insulin sensitivity and antioxidative ability, decreasing serum lipid.</p>

Improvement effects of puerarin on glycated brain damages in rats induced by D-galactose / 中国中药杂志

<p><b>OBJECTIVE</b>To observe the improvement effects of puerarin on glycated brain damages in rat model induced by D-galactose.</p><p><b>METHOD</b>The model rats of protein glycation were induced by intraperitoneal administration of D-galactose (150 mg x kg(-1) x d(-1)) for 8 weeks, and all rats were treated with puerarin (high dose 300 mg x kg(-1), middle dose 150 mg x kg(-1), low dose 75 mg x kg(-1)) for 6 weeks. The activity of aldose reductase in red blood cells, the amount of glycated products (fructosamine in serum, glycohaemoglobin, advanced glycation end-products) and AGEs in brain tissue, calcium ion in brain cells were measured. Moreover, mitochondria in brain hippocampus cells were observed under electronic microscope.</p><p><b>RESULT</b>High dose and middle dose of puerarin can decrease the activity of aldose reductase in red blood cells (P < 0.01), and inhibit the formation of glycation products significantly in model rats induced by D-galactose (P < 0.01). Also, puerarin can decrease the content of AGEs in brain and the level of calcium ions in brain cells (P < 0.05, P < 0.01), and decrease lesions degree in mitochondria in brain hippocampus cells.</p><p><b>CONCLUSION</b>Puerarin can produce the protective effects on glycated brain damages through inhibiting the glycation reaction in rats induced by D-galactose.</p>

Improvement effects of berberine on glycated brain damages in rats induced by D-galactose / 中成药

AIM: To observe the improvement effects of berberine on glycated brain damages in model rats induced by D-galactose. METHODS: The model rats of protein glycation were induced by intraperitoneal administration of D-galactose(150 mg/kg?d) for 8 weeks,and all rats were treated with berberine(high dose 300 mg/kg,middle dose 150 mg/kg,low dose 75 mg/kg) for 6 weeks.The activity of aldose reductase in red blood cells,the amount of glycated products(fructosamine in serum,glycohaemoglobin,advanced gtycation end-products),and the content of AGEs in brain tissue,calcium ion in brain cells were measured.Moreover,mitochondria in brain hippocampus cells were observed under electronic microscope. RESULTS: High dose and middle dose of berberine could decrease the activity of aldose reductase in red blood cells(P

Effect of puerarin on blood pressure and serum lipid in a rat model of insulin resistance / 中国病理生理杂志

AIM: To observe the effects of puerarin on blood pressure(BP),serum lipid in a rat model of insulin resistance and the mechanism.METHODS: Adult SD rats were maintained on high-fat-sugar-salt diet for 12 weeks.Puerarin was administered to the rats from 9th week for 4 weeks by intramuscular injection.BP was measured at the end of 0,8th,12th week.The levels of serum glucose,serum lipid,fasting serum insulin and the levels of MDA,TNF-?,plasma rennin,angiotensinⅡ(AngⅡ) and the activity of SOD were measured and the insulin-sensitivity index was also calculated at the end of the experiment.RESULTS: High and middle dosage of puerarin significantly decreased blood pressure,reduced the levels of serum lipid and AngⅡ,and also increased insulin-sensitivity index.The levels of MDA and TNF-? were significantly decreased by high dosage of puerarin.The activity of SOD was increased significantly.CONCLUSIONS: Puerarin possesses the effects of decreasing the blood pressure and serum lipid in a rat model of insulin resistance,which may be concerned with the changes of rennin-angiotensin system,the levels of oxygen-derived free radicals and TNF-?.

Antagonistic action of epigallocatechin-3-gallate on apoptosis in rat PC12 cells induced by 1-methyl-4-phenylpyridinium ion / 中国药理学通报

Aim To investigate the antagonistic action of EGCG on apoptosis of rat PC12 cell induced by MPP+.Methods PC12 cells were cultured and the apoptosis induced by MPP+(900 ?mol?L-1)was observed.The cells were randomly divided into 6 groups:blank group without any treatment,MPP+ control group,vitamin E group and EGCG groups(10,50,100 ?mol?L-1).After treatment of drugs,cell viability,leakage of LDH,morphological changes of mitochondria and apoptosis were detected by MTT,Hoechst 33342 staining,transmission electron microscope and flow cytometry,respectively.Results After treatment of cultured PC12 cells with MPP+,cell viability was decreased,leakage of LDH and apoptotic rate were increased,and mitochondria swelling,vacuole and cristae breakage were observed.Vitamin E and EGCG en-hanced cell viability,reduced the leakage of LDH and apoptotic rate,and decreased the damage degree of mitochondria.Conclusions EGCG possesses the ability of inhibiting rat PC12 cell apoptosis induced by MPP+,and its protective action may relate to its function of keeping mitochondria integrality.

Effects of epigallocatechin-3-gallate on 1-methyl-4-phenylpyridinium ion-induced apoptosis in rat PC12 cells / 中国病理生理杂志

AIM: To investigate the effects of epigallocatechin-3-gallate(EGCG) on 1-methyl-4-phenylpyridinium ion(MPP+)-induced apoptosis in rat pheochromocytoma(PC12) cells and to explore the relationships between its roles of anti-oxidation,intracellular calcium homeostasis and anti-apoptosis.METHODS: Rat PC12 cells were pretreated with vehicle control or EGCG(10,50,and 100 ?mol/L) for 30 min,then cultured with MPP+(900 ?mol/L) for 24 h.The cell viability and apoptosis were monitored by MTT assay and flow cytometry using Annexin V and PI.The activity of intracellular reactive oxygen species(ROS),contents of superoxide dismutase(SOD) and malondialdehyde(MDA),cytoplasmic Ca2+ density and apoptotic morphology of mitochondria were examined by fluorescent plate-based assays,confocal microscope,and transmission electron microscope,respectively.RESULTS: MPP+ impaired the PC12 cells in a concentration-dependent pattern and induced apoptosis of the cells(31% versus control).Compared with the control,the cells pretreated with EGCG showed markedly higher rate of viability and lower apoptosis.Meanwhile,EGCG pretreatment significantly increased the SOD activity and decreased the levels of MDA and ROS.Interestingly,EGCG also decreased the concentration of cytoplasmic Ca2+ and improved the morphology of mitochondria.CONCLUSION: EGCG exhibits inhibitory effects on MPP+-induced apoptosis in rat PC12 cells,which is possibly associated with increasing the cell ability of anti-oxidation and decreasing the concentration of cytoplasmic Ca2+.

A dopamine receptor antagonist modulates or enhances the analgesia of morphine and analysis of their synergetic analgesic mechanism / 中国病理生理杂志

AIM: To observe the synergetic analgesic effects of low dose of haloperidol, a dopamine antagonist and under-threshold dose of morphine on mice induced by thermal and acetic acid, and to analyze the major mechanism of their synergetic actions. METHODS: To examine the analgesic synergetic effect of haloperidol (0.315 mg/kg, 0.625 mg/kg, 1.25 mg/kg, ip respectively), morphine (3.125 mg/kg, 6.25 mg/kg, 12.5 mg/kg ip, respectively) or combining effect of haloperidol (0.3125 mg/kg) with morphine (3.125 mg/kg) on mice, we compared the change of pain threshold stimulated by thermal, latent period of twisting, the number of times of twisting by acetic acid, and we also estimated the antagonistic effect of d -amphetamine (10 mg/kg) and naloxone (5 mg/kg) on haloperidol and morphine group. RESULTS: Combination of haloperidol with morphine significantly enhanced pain threshold of mice induced by thermal, prolonged latent period of twisting and decreased the number of times of twisting. Naloxone markedly antagonized the combination of analgesic action of haloperidol and morphine and not d -amphetamine. CONCLUSION: Combination of haloperidol with morphine have synergetic analgesic effect and morphine is the dominant factor.

THE PROTECTIVE EFFECT OF TEA POLYPHENOLS ON RENAL DAMAGE IN RATS INDUCED BY D-GALACTOSE AND ITS MECHANISM / 营养学报

Objective To investigate the effect of tea polyphenols (TP) on renal damage in rats model induced by D-galactose. Methods Rats were injected with D-galactose (150 mg/kg?d),ip for 8 w,to induce renal damage. From the 3rd week,TP (150,75,37.5 mg/kg?d),aminoguanidine (150 mg/kg) and vitamin E (150 mg/kg) were administered with D-galactose for 6 w. After treatment,fasting blood glucose and 2 h blood glucose in oral glucose tolerance test were measured. The levels of HbA1C and fructosamine in serum,the activity of aldose reductase and content of advanced glycation end products (AGEs) in plasma and in kidney tissues and the activity of SOD,GSH-Px,and the contents of MDA in kidney tissues were measured,and 24h urinary protein,blood urea nitrogen (BUN) and serum creatinine (Cr) were detected. The apoptosis of renal cells were detected by flow cytometer. Results After treatment of D-galactose for 8 w,2h glucose level in oral glucose talerance test was increased significantly,the activity of aldose reductase and the content of AGES were increased significantly in blood. The levels of AGEs and MDA in renal tissues were also enhanced significantly. However,the activities of SOD and GSH-Px decreased. Additionally,the contents of 24h urine protein,BUN,Cr and the apoptotic rate of renal cells were increased significantly. High and middle dose of TP could can decrease the activity of aldose reductase in red blood cells,and inhibit the formation of glycation products in model rats induced by D-galactose. Also,TP could enhance the antioxidative activities and decrease the contents of AGEs and MDA in renal tissues. Mesnwhile,24h urine protein,BUN and Cr and the apoptotic rate of renal cells were increased significantly. Conclusion TP can inhibit glycation reaction induced by D-galactose and then protect renal from damage caused by glycation.