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.

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The aim of this study was to evaluate the effect of naringin on experimentally induced inflammatory bowel disease in rats. Naringin (20, 40 and 80 mg/kg) was given orally for 7 days to Wistar rats before induction of colitis by intrarectal instillation of 2 mL of 4% (v/v) acetic acid solution. The degree of colonic mucosal damage was analyzed by examining mucosal damage, ulcer area, ulcer index and stool consistency. Intrarectal administration of 4% acetic acid resulted in significant modulation of serum alkaline phosphatase, lactate dehydrogenase, superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) content along with colonic nitric oxide (NO), xanthine oxidase (XO) level and protein carbonyl content in the colonic tissue as well as in blood. Naringin (40 and 80 mg/kg) exerted a dose dependent (P < 0.05) ameliorative effect, as it significantly increased hematological parameter as well as colonic SOD and GSH. There was a significant (P < 0.05) and dose dependant inhibition of macroscopical score, ulcer area along with colonic MDA, MPO activity by the 7 days of pretreatment of naringin (40 and 80 mg/kg). Biochemical studies revealed a significant (P < 0.05) dose dependant inhibition in serum alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) levels by pretreatment of naringin. Increased levels of colonic NO, XO, protein carbonyl content and DNA damage were also significantly decreased by naringin pretreatment. The findings of the present investigation propose that naringin has an anti-inflammatory, anti-oxidant and anti-apoptotic potential effect at colorectal sites as it modulates the production and expression of oxidative mediators such as MDA, MPO, NO and XO, thus reducing DNA damage.

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