In this paper, the protective effect of the bioflavonoid quercetin on behaviors, antioxidases, and neurotransmitters in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-(MPTP-) induced Parkinson's disease (PD) was investigated. Quercetin treatment (50 mg/kg, 100 mg/kg and 200 mg/kg body weight) was orally administered for 14 consecutive days. The results show that quercetin treatment markedly improves the motor balance and coordination of MPTP-treated mice. Significant increases were observed in the activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and Na+, K+-ATPase, AchE, the content of dopamine (DA) in the quercetin plus MPTP groups compared to those in the MPTP group. Significant reduction the 4-hydroxy-2-nonenal (4-HNE) immunoreactivity in striatum of brains was observed in the quercetin plus MPTP groups in comparison to the MPTP group. Taken together, we propose that quercetin has shown antiparkinsonian properties in our studies. More work is needed to explore detailed mechanisms of action.

The first two authors contributed equally to this work KMUP-l increases nitric oxide (NO) via endothelium nitric-oxide synthase (eNOS). Deficiency of eNOS and peroxisome proliferator-activated receptor-y (PPARy) is the pathogenesis of diabetic nephropathy (DN). This study aims to investigate whether KMUP-l inhibits streptozotocin (STZ)-induced proinflammation in early DN. In experiments, STZ was used to induce diabetes in Wistar rats. Twenty-four male rats were randomly divided into four groups, including control, STZ (65 mg/kg, Lp.), STZ+KMUP-l(l mg/kg) and STZ+KMUP-l (2.5 mg/kg). KMUP-l HCI was dissolved in distilled water for oral administration. The morphology of renal tissues was evaluated by periodic acid-schiff(PAS) staining and immunohistochemistry of eNOS. The expressions of matrix metalloproteinase-2/-9 (MMP-2/-9), eNOS, B-celllymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and PPARy of renal tissues were examined by Western blotting technique. NO production was evaluated by Griess reagent. Oxidative stress was evaluated by measuring reactive oxygen species (ROS). Results indicated that STZ-induced diabetic mellitus (DM) and subsequent DN, including excessive deposition of extracellular matrix (ECM) accompanied by enhanced MMP-2/-9, raised ROS production, increased Bcl-2/Bax ratio and decreased eNOSIPPARy over a period of 4 weeks. KMUP-1 inhibited STZ-induced hyperglycemia, BUN, MMP-2IMMP-9, and restored eNOS-PPARy expression in renal tissues. Immunohistochemistry (lHC) of eNOS in glomeruli of renal cortical tissue sections indicated that KMUP-l restored the eNOS caused by STZ. PAS staining of glomeruli indicated that KMUP-l could not significantly reduce STZ-induced ECM expansion. Moreover, KMUP-l increased Bcl-2/Bax and decreased ROS. In summary, KMUP-l inhibits STZ-induced proinflammation in early DN by restoring PPARy/eNOS and inhibiting MMP-9. Natural source xanthine-based KMUP-l, (7-[2-[4-(2-hlorophenyl) piperazinyl] ethyl]-I, 3-di-methyl xanthine (Fig. I), has increased eNOS/cyclic guanosine monophosphate (cGMP) in cardiovascular system (1-3). These results encouraged us to determine whether KMUP-I could protect kidney from STZ-induced diabetes mellitus (DM) and associated diabetic nephropathy (DN) via