Algal acid oligosaccharide HS971 is a seaweed extract. Studies have shown that oligosaccharides have protective effects on neuronal damage, and the algae polysaccharides, which are also seaweed extracts, have been experimentally proven to be able to nourish nerve cells and significantly improve the survival rate of cultured nerve cells. In this study, the effects of HS971 on the release of dopamine in striatum and amygdala were observed in Parkinson's model rats prepared with 6-hydroxydopamine, and the regulation of HS971 on the function of dopaminergic neurons in Parkinson's rats was studied.
Rats of standard Parkinson's model were randomly divided into two groups. One group was intraperitoneally injected with 5 mg·kg·d- of brown algae acid oligosaccharide HSH971 for 7 days; the other group was intraperitoneally injected with the same volume and time course of normal saline as control. Results After intraperitoneal injection of brown algae acid oligosaccharide HS971 5 mg·kg·d - 7 days, the release of dopamine from the striatum of Parkinson's rats was significantly higher than that of the control group. There was no significant difference in dopamine release between the two groups of healthy striatum. The effect of intraperitoneal injection of brown algae acid oligosaccharide HS971 on the release of dopamine from amygdala is similar to that of striatum. The amount of dopamine released from the amygdaloid nucleus in the HS971 group was significantly higher than that in the saline-controlled group. However, no significant difference was found in the amygdala release from the healthy side of the two groups.
This experiment showed that after treatment with HS971, Parkinson's model rats showed a significant increase in dopamine release from the striatum and amygdala, but no significant changes in the healthy side. Therefore, HS971 is important for the repair of dopaminergic neurons after injury. The regulation of HS971 on the release of dopamine from the damaged striatum and amygdala may be related to improving the metabolic function of residual dopaminergic neurons, ie, enhancing dopamine synthase activity or inhibiting dopamine reuptake.