ABSTRACT
Objective To investigate the expression of peroxisome proliferator-activated receptors (PPARs) α/δ/γ protein and the effect of berberine on them in diabetic rat kidney.Methods Type 2 diabetic rats were induced by injection (ip) with streptozotocin 35 mg·kg1 and feeding with a high-carbohydrate/high-fat diet for 16 weeks.From week 17 to 32, diabetic rats were given low, middle, high-dose berberine 75, 150, 300 mg×kg-1, fenofibrate 100 mg×kg1 and rosiglitazone 4 mg×kg-1, respectively.The expression of PPARα/δ/γ protein in kidney were detected by immunohistochemistry.Results The expression of PPARα and PPARδ protein in the kidney of diabetic rat, which were significantly higher than that of the control one (P＜0.01), while PPARγ expression was obviously lower than that of the control one (P＜0.01).The expression of PPARα and PPARδ in in diabetic kidney were increased notably after middle-dose, high-dose berberine and fenofibrate treatment (P＜0.01);middle-dose, high-dose berberine and rosiglitazone treatment significantly reduced PPARγ expression (P＜0.01).Conclusion Berberine can restore the disturbed PPARα/δ/γ protein expression in diabetic rat kidney.
ABSTRACT
Objective To investigate the expression of peroxisome proliferator-activated receptors (PPARs) α/δ/γ protein and the effect of berberine on them in diabetic rat kidney.Methods Type 2 diabetic rats were induced by injection (ip) with streptozotocin 35 mg·kg1 and feeding with a high-carbohydrate/high-fat diet for 16 weeks.From week 17 to 32, diabetic rats were given low, middle, high-dose berberine 75, 150, 300 mg×kg-1, fenofibrate 100 mg×kg1 and rosiglitazone 4 mg×kg-1, respectively.The expression of PPARα/δ/γ protein in kidney were detected by immunohistochemistry.Results The expression of PPARα and PPARδ protein in the kidney of diabetic rat, which were significantly higher than that of the control one (P＜0.01), while PPARγ expression was obviously lower than that of the control one (P＜0.01).The expression of PPARα and PPARδ in in diabetic kidney were increased notably after middle-dose, high-dose berberine and fenofibrate treatment (P＜0.01);middle-dose, high-dose berberine and rosiglitazone treatment significantly reduced PPARγ expression (P＜0.01).Conclusion Berberine can restore the disturbed PPARα/δ/γ protein expression in diabetic rat kidney.
ABSTRACT
Retinopathy is a major cause of morbidity in diabetes and remains the primary cause of new blindness. Therefore, it is necessary to find new drug to treat diabetic retinopathy. Type 2 diabetes mellitus (T2DM) rats were induced by injection (ip) with streptozotocin (STZ) 35 mg x kg(-1) and fed with a high-carbohydrate/high-fat diet 2 weeks later. From week 17 to 32, diabetic rats were given different doses of berberine 75, 150, and 300 mg x kg(-1), fenofibrate 100 mg x kg(-1) and rosiglitazone 4 mg x kg(-1), separately. Retinal structure was observed with hematoxylin-eosin staining and peroxisome proliferator-activated receptors (PPARs) alpha/delta/gamma protein expressions were detected by immunohistochemistry. The retina of control rats was thicker than that of other groups, 16 weeks treatment with berberine (150 and 300 mg x kg(-1)) and rosiglitazone 4 mg x kg(-1) thickened the diabetic retina, but no difference existed in retinal structure among groups. Both berberine (150 and 300 mg x kg(-1)) and rosiglitazone 4 mg x kg(-1) significantly decreased PPARy expression in diabetic retina; while berberine (150 and 300 mg x kg(-1)) and fenofibrate 100 mg x kg(-1) obviously increased both PPARalpha and PPARdelta expressions in diabetic retina. Berberine modulates PPARalpha/delta/gamma protein levels in diabetic retina which may contribute to ameliorate retinopathy complication induced by STZ and a high-carbohydrate/high-fat diet. It is expected that berberine might be a more beneficial drug to treat diabetic retinal complication comparing with fenofibrate and rosiglitazone.
Subject(s)
Animals , Male , Rats , Berberine , Pharmacology , Diabetes Mellitus, Experimental , Metabolism , Diabetes Mellitus, Type 2 , Metabolism , Diabetic Retinopathy , Metabolism , Fenofibrate , Pharmacology , Hypoglycemic Agents , Pharmacology , PPAR alpha , Metabolism , PPAR delta , Metabolism , PPAR gamma , Metabolism , Rats, Wistar , Retina , Metabolism , Pathology , Thiazolidinediones , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To evaluate the effects of Caulis Sinomenii and sinomenine on conditioned place preference (CPP) induced by morphine and brain histamine level in mice.</p><p><b>METHODS</b>Sixty mice were randomized into 6 equal groups and morphine (Mor) was injected subcutaneously (9 mg/kg) for 6 consecutive days to induce CPP using a shuttle box. Since the 4th day of training, the mice in 5 of the groups were treated for 3 consecutive days with Caulis Sinomenii (10 g/kg), sinomenine (60 mg/kg), diphenhydramine (30 mg/kg), CP48/80 (5 mg/kg) and L-histidine (750 mg/kg) in addition to morphine (9 mg/kg) treatment, respectively, leaving the other group with exclusive morphine treatment. Another 10 mice received saline injection to serve as saline control group. The content of histamine (HA) in the mouse brain was measured by fluorospectrophotometry.</p><p><b>RESULTS</b>In morphine group, the mice showed significantly extended stay in morphine-paired compartment whose HA content in the brain was markedly increased (P<0.01). Treatment with Caulis Sinomenii and sinomenine resulted in significantly reduced time of stay in morphine-paired compartment and brain HA level (P<0.01).</p><p><b>CONCLUSION</b>CPP induced by morphine in mice is associated with increased HA level in the brain. Caulis Sinomenii and sinomenine can suppress the acquisition of place preference induced by morphine and modulate HA level in the central nervous system in morphine-dependent mice.</p>