ABSTRACT
Objective:To observe the clinical efficacy of modified Buyang Huanwutang combined with electroacupuncture （EA） in the treatment of traumatic spinal cord injury （TSCI） due to Qi deficiency and blood stasis. Method:Eighty-seven TSCI patients who met the inclusion requirements were randomly divided into an observation group （<italic>n</italic>=44） and a control group （<italic>n</italic>=43）. On the basis of comprehensive western medical treatments， patients in the control group were further provided with Wuwei Tongshuan oral liquid，10 mL per time，three times per day， while those in the observation group received modified Buyang Huanwutang，one bag per day，for 12 consecutive weeks. Besides， EA was performed in both groups in the same way， once per day， six times per week， for six weeks in total. The American Spinal Injury Association （ASIA） motor score， modified Barthel index （MBI），visual analog scale （VAS） pain score，Berg balance scale （BBS） score，modified Ashworth scale （MAS） score， spinal cord independence measure-Ⅲ（SCIM-Ⅲ） score， lower limb range of motion （ROM）， and Qi deficiency and blood stasis syndrome score before and after treatment were evaluated， followed by the recording of the occurrence of complications during treatment. The brain-derived nerve growth factor （BDNF）， nerve growth factor （NGF）， vascular endothelial growth factor （VEGF）， neurotrophic factor-3 （NT-3）， malondialdehyde （MDA） and superoxide dismutase （SOD） levels before and after treatment were determined. Result:The motor， light touch， needling sensation， MBI， and BBS scores of the observation group were higher than those of the control group （<italic>P</italic><0.01）， while the AS and MAS scores were lower（<italic>P</italic><0.01）. The angles of adductor and straight leg raising in the observation group were greater than those of the control group （<italic>P</italic><0.01），but the Qi deficiency and blood stasis syndrome score was lower（<italic>P</italic><0.01）. Both the scores of self-care， respiration， and sphincter management in SCIM-Ⅲ and the total score in the observation group were elevated as compared with those of the control group （<italic>P</italic><0.01）. The cumulative incidence of complications in the observation group was 34.09%，significantly lower than 55.81% in the control group （<italic>χ</italic><sup>2</sup>=4.149，<italic>P</italic><0.05）. Compared with the control group， the observation group exhibited remarkably increased BDNF， NGF， VEGF， NT-3， and SOD （<italic>P</italic><0.01） and decreased MDA （<italic>P</italic><0.01）. Conclusion:Modified Buyang Huanwutang combined with EA is effective in alleviating spinal cord injury， promoting neural functional recovery， improving independence in activities of daily living， reducing the incidence of complications of patients with TSCI， which may be related to the amelioration of ischemia and hypoxia， inhibition of lipid peroxidation， and acceleration of nerve cell repair and regeneration.
ABSTRACT
There are numerous mechanisms by which the brain generates seizures. It is well known that oxidative stress plays a pivotal role in status epilepticus (SE). Salidroside (SDS) extracted from Rhodiola rosea L. shows multiple bioactive properties, such as neuroprotection and antioxidant activity in vitro and in vivo. This study explored the role of SDS in kainic acid (KA)-induced SE and investigated the underlying mechanism. Latency to SE increased in the SDS-pretreated mice compared to the KA group, while the percentage of incidence of SE was significantly reduced. These results suggested that pretreatment with SDS not only delayed SE, but it also decreased the incidence of SE induced by KA. KA increased MDA level and reduced the production of SOD and GSH at multiple timepoints after KA administration. SDS inhibited the change of MDA, SOD and GSH induced by KA prior to SE onset, indicating that SDS protects against KA-induced SE via suppressing oxidative stress. Based on these results, we investigated the possible molecular mechanism of SDS. Pretreatment with SDS reversed the KA-induced decrease in AMP-activated protein kinase (AMPK); increased the sirtuin 1 (SIRT1) deacetylase activity in KA-treated mice, which had no demonstrable effect on SIRT1 mRNA and protein; and suppressed the KA-induced increase in Ace-FoxO1. These results showed that AMPK/SIRT1/FoxO1 signaling is possibly the molecular mechanism of neuroprotection by SDS.