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| Effects of astragalus polysaccharide on post-stroke depression in rats |
| LIU Lizhu1 LIU Wei2 FAN Lin2 GUO Lihong1 |
1.Department of Sleep Disorders Center, Taihe Hospital Affiliated Hospital of Hubei University of Medicine, Hubei Province, Shiyan 442000, China;
2.Ward Two, Department of Orthopedics Rehabilitation, Taihe Hospital Affiliated Hospital of Hubei University of Medicine, Hubei Province, Shiyan 442000, China |
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Abstract Objective To investigate the effects and possible mechanism of astragalus polysaccharide (APS) on post-stroke depression (PSD) in rats. Methods Wistar rats were screened by open field test, and a total of 48 eligible rats were divided into blank control group, model control group, APS low dose group and APS high dose group according to random number table method, with 12 rats in each group. The model of focal cerebral ischemia was established using suture-occluded method in all groups except the blank control group, and the rat PSD model was established by isolation housing combined with chronic unpredictable stress method (CUMS). Post-surgery, rats received treatment of APS 200 mg/(kg·d) (APS low dose group), APS 400 mg/(kg·d) (APS high dose group) and equal volume of saline (model control group and blank control group) for 4 weeks by gavage. Results from the behavioral and electrophysiology experiments, and the level of protein and gene expressions of nuclear factor-κB (NF-κB) and peroxisome proliferator-activated receptor-gamma (PPAR-γ) in hippocampal CA1 region were analyzed to determine the effect of APS on PSD in rats. Results Compared with the model control group, the APS low dose group and the APS high dose group showed significantly lower spontaneous action potential (AP) and group peak potential (PS) voltages in the CA1 region by patch clamp recordings, significantly lower NF-κB protein and mRNA expression and significantly higher PPAR-γ protein and mRNA expression, the differences were statistically significant (P ＜ 0.05). The saccharification water intake experiment showed that the sucrose intake of the two APS dose groups were significantly higher than those of the model control group, the water maze test showed that the escape latency of the rats in the two APS dose groups were significantly shortened and number of platform crossings were significantly increased, the differences were statistically significant (P ＜ 0.05). The changes of the above parameters in the APS high dose group were more obvious than those in the APS low dose group, the differences were statistically significant (P ＜ 0.05). Conclusion APS may play a therapeutic role in PSD by inhibiting the phosphorylation of NF-κB signaling pathway and stabilizing the AP and PS voltages in the hippocampal CA1 region.
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