Details

Autor(en) / Beteiligte

• Kandhare, Amit D
• Shivakumar, V
• Rajmane, Anuchandra
• Ghosh, Pinaki
• Bodhankar, Subhash L

Titel

Evaluation of the neuroprotective effect of chrysin via modulation of endogenous biomarkers in a rat model of spinal cord injury

Ist Teil von

• Journal of natural medicines, 2014-07, Vol.68 (3), p.586-603

Ort / Verlag

Tokyo: Springer-Verlag

Erscheinungsjahr

2014

Link zum Volltext

Quelle

SpringerLink

Beschreibungen/Notizen

• The objective of the present investigation was to evaluate the neuroprotective efficacy of chrysin in an experimental rat model of spinal cord injury (SCI). SCI was induced in male Sprague–Dawley rats by placing an aneurysm clip extradurally for 60 s at T10. The rats received treatment with either vehicle (SCI control) or chrysin (10, 20 and 40 mg/kg, p.o.) for 28 days. The various behavioral, biochemical and molecular parameters were determined. Chronic treatment with chrysin (20 and 40 mg/kg) significantly and dose-dependently (P < 0.05) attenuated the decrease in body weight, urine output, footprint analysis, sperm count and organ weight (testis, seminal vesicle and urinary bladder). It significantly improved (P < 0.05) the nociceptive threshold, motor and sensory nerve conduction velocity. The decreased activity of superoxide dismutase, reduced glutathione and membrane-bound inorganic phosphate were significantly (P < 0.05) restored by chrysin treatment. SCI resulted in a significant increase (P < 0.05) in lipid peroxidase, nitric oxide, tumor necrosis factor alpha, interleukin-1β, and bax whereas expression of bcl-2 and caspase-3 were significantly (P < 0.05) reduced. These changes were significantly reduced by treatment with chrysin (20 and 40 mg/kg, P < 0.05). Histological aberration induced after SCI in spinal cord, testis, kidney and urinary bladder were restored by treatment with chrysin (20 and 40 mg/kg). In conclusion, chrysin is a potential flavone-possessing antioxidant and its antiapoptotic property caused the subsequent recovery of both motor and sensory functions via modulation of endogenous biomarkers and neuronal apoptosis to inhibit the incidence of neurological deficits due to SCI.