mobic and Parkinsonian-Disorders

Recent experimental and clinical studies on Parkinson's disease point out the pivotal role of inflammation in the pathogenesis of neurodegeneration and the possible positive effects of nonsteroidal anti-inflammatory drug therapies. Our aim in this study was to investigate the preventive effects of nonsteroidal anti-inflammatory drugs in the 6-hydroxydopamine (6-OHDA) induced rat model of Parkinson's disease.. Twenty-one female Wistar-Albino rats (200-250g) were used in this study. The rats were divided in three groups: Saline group (n: 7, 2 ml), Acetylsalicylic acid group (n: 7, 100 mg/kg), and Meloxicam group (n: 7, 50 mg/kg). An hour after administration, the rats received a unilateral intranigral injection of 6-OHDA to produce the Parkinson model lesion. Rotational tests were performed two weeks later as follow-up. Immunohistochemical tests were performed in all groups to determine the severity of the lesion in the substantia nigra.. Administration of drugs an hour before the lesions were created did not protect the degeneration of dopaminergic neurons in the substantia nigra.. Oral usage of low repeated doses of nonsteroidal anti-inflammatory drugs may possibly slow down the progression of the disease.

Topics: Amphetamines; Animals; Antiparkinson Agents; Apomorphine; Aspirin; Behavior, Animal; Cyclooxygenase Inhibitors; Disease Models, Animal; Female; Immunohistochemistry; Meloxicam; Neuroprotective Agents; Oxidopamine; Parkinsonian Disorders; Rats; Rats, Wistar; Sympatholytics; Thiazines; Thiazoles

To study the possible role of the isoenzymes of cyclooxygenase COX-1 and COX-2 in the MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse model of Parkinson's disease we used acetylsalicylic acid, a COX-1/COX-2 inhibitor, in comparison with meloxicam, a preferential COX-2 inhibitor. As markers of protection we determined the effects on MPTP-induced striatal dopamine depletion, locomotor activity, cell loss, and tyrosine hydroxylase immunoreactivity (TH-IR) in the substantia nigra pars compacta. Male C57BL/6 mice (n = 82) were treated with a single dose of acetylsalicylic acid (10, 50, 100 mg/kg i.p.) or meloxicam (2, 7.5, 50 mg/kg i.p.) immediately prior to administration of MPTP (30 mg/kg s.c.) or saline. After 7 days the mice were sacrificed to analyze striatal dopamine and metabolite levels. Nigral sections were processed for Nissl-staining and TH-IR. In the saline-treated MPTP control group striatal dopamine levels were reduced to 15.9% of control values. Dopamine depletion was significantly attenuated to values of 37.1 and 38.6% of saline control values by acetylsalicylic acid (50 and 100 mg/kg) and to values of 36 and 40% by meloxicam (7.5 and 50 mg/kg), respectively. MPTP-induced decrease of locomotor activity was significantly attenuated by acetylsalicylic acid and meloxicam. Remarkably, the MPTP-induced decrease of TH-IR as well as the loss of nigral neurons was nearly completely prevented by acetylsalicylic acid (100 mg/kg) and meloxicam (7.5 and 50 mg/kg). In conclusion, the inhibition of either COX-1/COX-2 by acetylsalicylic acid or preferentially COX-2 by meloxicam provided a clear neuroprotection against MPTP-toxicity on the striatal and nigral levels.

Topics: 1-Methyl-4-phenylpyridinium; 3,4-Dihydroxyphenylacetic Acid; Animals; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Cell Count; Cyclooxygenase 1; Cyclooxygenase 2; Disease Models, Animal; Dopamine; Homovanillic Acid; Isoenzymes; Male; Meloxicam; Membrane Proteins; Mice; Mice, Inbred C57BL; Motor Activity; Neostriatum; Neuroprotective Agents; Parkinsonian Disorders; Prostaglandin-Endoperoxide Synthases; Substantia Nigra; Thiazines; Thiazoles; Tyrosine 3-Monooxygenase