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1.
Asian Pacific Journal of Tropical Biomedicine ; (12): 205-213, 2021.
Artículo en Chino | WPRIM | ID: wpr-883381

RESUMEN

Objective: To investigate the effect of aloin against chronic constriction injury (CCI)-induced neuropathic pain in rats. Methods: Rats were randomly divided into 7 groups: Group Ⅰ (normal control), Group Ⅱ (sham-operated), Group Ⅲ (CCI control) and Group Ⅳ, Ⅴ, Ⅵ, and Ⅶ, which underwent CCI surgery and then were administered with aloin (5 mg/kg, p.o.; 25 mg/kg, p.o.; 125 mg/kg, p.o.) and gabapentin (50 mg/kg, p.o.), respectively for 14 days. Peripheral neuropathy was induced by silk ligatures (4-0) loosely placed around the sciatic nerve. Nociceptive thresholds against mechanical stimuli (Von-Frey filaments) and thermal stimuli (12 ℃ and 40 ℃) were measured at mid-plantar paw region ipsilateral to the compressed nerve on day-3, 7, 11, and 14. The concentration of cytokines including tumor necrosis factor-α (TNF-α), interleukin-6, and interleukin-1β was estimated at day-7. At day 14, motor nerve conduction velocity was determined under urethane anesthesia (1.25 g/kg). Oxidative stress parameters (malondiadehyde, glutathione, catalase, and superoxide dismutase) were estimated in sciatic nerve homogenates at day 14. Representative nerve samples were processed for histological investigations. Results: Aloin significantly reduced CCI-induced mechanical and thermal allodynia. It also improved motor nerve conduction velocity and decreased oxidative stress in nerve tissues. In addition, it decreased pro-inflammatory cytokine levels and restored the histoarchitecture of compressed sciatic nerve. Conclusions: Aloin mitigates CCI-induced neuropathic pain in rats by inhibiting oxidative stress and pro-inflammatory cytokines in the afflicted sciatic nerve.

2.
Asian Pacific Journal of Tropical Biomedicine ; (12): 797-804, 2017.
Artículo en Chino | WPRIM | ID: wpr-664242

RESUMEN

Objective:To determine whether corosolic acid (CA) targeting nuclear protein expression of Nrf2 activation can be used to attenuate renal damage and preserve renal function in alloxan diabetic mice.Methods:A mouse model with diabetic nephropathy was established to examine the Nrf2 expression.Mice were randomly divided into control,diabetic control,and CA groups treated at 0.4 mg/kg,2 mg/kg and 10 mg/kgp.o.for 8 weeks.Diabetes was induced in mice by single intraperitoneal injection of alloxan 200 mg/kg in all groups except the control.The mice with fasting blood glucose level over 200 mg/dL were considered as diabetic and were employed in the study.After 4th and 8th weeks,urine samples were collected (using metabolic cages) to measure protein and urea.Animals were euthanized,and serum samples were collected to estimate the glucose,creatinine,total protein,urea and blood urea nitrogen.Kidney was isolated at the end of experiment for histology to evaluate anti-oxidant parameters.Immunohistochemistry was performed to examine the Nrf2 expression.Results:CA treatment showed dose dependent reduction in level of biochemical parameters in serum and urine.CA group (10 mg/kg) showed significantly higher body weight and reduced kidney weight.Histopathological examination revealed reduced inflammation,collagen deposition and glomerulosclerosis in renal tissue.CA attenuated renal dysfunction,oxidative stress and inflammatory pro-cytokine levels.Conclusions:CA treatment exhibited ameliorative effect on kidney in mice with its enhanced Nrf2 expression.

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