Abstract

To study the effects of astaxanthin on the apoptosis after spinal cord injury in rats. One hundred and forty-four healthy adult Sprague Dawley rats were divided into experimental group, control group, and sham group according to the random number table ( n=48). In the control group and the experimental group, the modified Allen's method was used to make the spinal cord injury model; in the sham group, only the lamina was cut without damaging the spinal cord. At immediate after operation, the rats in the experimental group were given intragastric administration of astaxanthin (75 mg/kg) twice a day; and the rats in the control group and the sham group were given equal amount of olive oil by gavage twice a day. BBB score was used to assess the motor function at 1 day and 1, 2, 3, and 4 weeks after operation. The malondialdehyde (MDA) content was determined by the thiobarbituric acid method at 24 hours after operation; and the activity of superoxide dismutase (SOD) was determined by the xanthine oxidase method. Apoptosis index (AI) was determined by TUNEL method at 6, 24, and 48 hours after operation. At 48 hours after operation, the water content of spinal cord was measured by dry-wet weight method, the lesion ratio of spinal cord was calculated, the ultrastructure of the spinal cord was observed by transmission electron microscopy, and ultrastructure scoring was performed using the Kaptanoglu score method. The BBB score in the control group and the experimental group was significantly lower than that in the sham group at each postoperative time point ( P<0.05); and the BBB score in the experimental group were significantly higher than that in the control group at 1-4 weeks postoperatively ( P<0.05). The MDA content in the control group and the experimental group was significantly higher than that in the sham group at 24 hours after operation, and in the experimental group was significantly lower than in the control group ( P<0.05). The SOD activity in the control group and the experimental group was significantly lower than that in the sham group, and in the experimental group was significantly higher than in the control group ( P<0.05). At each time point postoperatively, the AI in the control group and the experimental group was significantly higher than that in the sham group, and in the experimental group was significantly lower than in the control group ( P<0.05). At 48 hours after operation, the water content of spinal cord, the lesion ratio of spinal cord, and the ultrastructure score in the control group and the experimental group were significantly higher than those in the sham group, and in the experimental group were significantly lower than in the control group ( P<0.05). Astaxanthin can inhibit the lipid peroxidation, reduce the apoptosis, reduce the spinal cord edema, reduce the spinal cord lesion, reduce the histopathological damage after spinal cord injury, and improve the motor function of rats with spinal cord injury, and protect the spinal cord tissue, showing an obvious neuroprotective effect.

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