TY - JOUR
T1 - Dose-dependent neuroprotective effect of caffeine on a rotenone-induced rat model of parkinsonism: A histological study
AU - Soliman, Amira M.
AU - Fathalla, Ahmed M.
AU - Moustafa, Ahmed A.
PY - 2016/6/3
Y1 - 2016/6/3
N2 - Several lines of evidence have demonstrated an inverse relationship between caffeine utilization and Parkinson's disease (PD) progression. Caffeine is a methylxanthine known as a non-specific inhibitor of adenosine (A2A and A1) receptors in the cerebrum and demonstrated to be a neuroprotective medication. In this study, the neuroprotective efficacy of two different doses of caffeine ranging above the usual consumption dose and below the toxic dose was investigated using histopathological and immunohistochemical methods. Thirty-two male rats were randomly divided into 4 groups, with 8 in each group: vehicle control (1 ml/kg/48 h for 12 days), rotenone (1.5 mg/kg/48 h, s.c. for 12 days), low-dose Caffeine-treated: (10 mg/kg IP. daily for 12 days), high-dose Caffeine-treated (20 mg IP daily for 12 days). Twenty-four hours after the last rotenone injection, animals were sacrificed and brains were sectioned and prepared for histopathological staining with hematoxylinand eosin, cresyl violet and Mallory's phosphotungestic acid haematoxylinand for immunohistochemical staining of tyrosine hydroxylase. Our study showed that the treatment with caffeine improved histopathological degeneration in the substantia nigra parts compacta (SNpc) neurons and hindered the reduction in dopamine concentration caused by rotenone. We also found that a higher dose of caffeine was more effective against histopathological degeneration. These results suggest that caffeine has a dose-dependent neuroprotective effect.
AB - Several lines of evidence have demonstrated an inverse relationship between caffeine utilization and Parkinson's disease (PD) progression. Caffeine is a methylxanthine known as a non-specific inhibitor of adenosine (A2A and A1) receptors in the cerebrum and demonstrated to be a neuroprotective medication. In this study, the neuroprotective efficacy of two different doses of caffeine ranging above the usual consumption dose and below the toxic dose was investigated using histopathological and immunohistochemical methods. Thirty-two male rats were randomly divided into 4 groups, with 8 in each group: vehicle control (1 ml/kg/48 h for 12 days), rotenone (1.5 mg/kg/48 h, s.c. for 12 days), low-dose Caffeine-treated: (10 mg/kg IP. daily for 12 days), high-dose Caffeine-treated (20 mg IP daily for 12 days). Twenty-four hours after the last rotenone injection, animals were sacrificed and brains were sectioned and prepared for histopathological staining with hematoxylinand eosin, cresyl violet and Mallory's phosphotungestic acid haematoxylinand for immunohistochemical staining of tyrosine hydroxylase. Our study showed that the treatment with caffeine improved histopathological degeneration in the substantia nigra parts compacta (SNpc) neurons and hindered the reduction in dopamine concentration caused by rotenone. We also found that a higher dose of caffeine was more effective against histopathological degeneration. These results suggest that caffeine has a dose-dependent neuroprotective effect.
UR - http://www.scopus.com/inward/record.url?scp=84965076819&partnerID=8YFLogxK
U2 - 10.1016/j.neulet.2016.04.057
DO - 10.1016/j.neulet.2016.04.057
M3 - Article
C2 - 27132082
AN - SCOPUS:84965076819
SN - 0304-3940
VL - 623
SP - 63
EP - 70
JO - Neuroscience Letters
JF - Neuroscience Letters
ER -