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Salidroside protects against kainic acid-induced status epilepticus via suppressing oxidative stress.
Neurosci Lett. 2016 Apr 08; 618:19-24.NL

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.

Authors+Show Affiliations

Key Laboratory of Neurology of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050071, PR China.Key Laboratory of Neurology of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050071, PR China.Key Laboratory of Neurology of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050071, PR China.Key Laboratory of Neurology of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050071, PR China.Key Laboratory of Neurology of Hebei Province, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050071, PR China. Electronic address: wpwang203@163.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26940236

Citation

Si, Pei-Pei, et al. "Salidroside Protects Against Kainic Acid-induced Status Epilepticus Via Suppressing Oxidative Stress." Neuroscience Letters, vol. 618, 2016, pp. 19-24.
Si PP, Zhen JL, Cai YL, et al. Salidroside protects against kainic acid-induced status epilepticus via suppressing oxidative stress. Neurosci Lett. 2016;618:19-24.
Si, P. P., Zhen, J. L., Cai, Y. L., Wang, W. J., & Wang, W. P. (2016). Salidroside protects against kainic acid-induced status epilepticus via suppressing oxidative stress. Neuroscience Letters, 618, 19-24. https://doi.org/10.1016/j.neulet.2016.02.056
Si PP, et al. Salidroside Protects Against Kainic Acid-induced Status Epilepticus Via Suppressing Oxidative Stress. Neurosci Lett. 2016 Apr 8;618:19-24. PubMed PMID: 26940236.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Salidroside protects against kainic acid-induced status epilepticus via suppressing oxidative stress. AU - Si,Pei-Pei, AU - Zhen,Jun-Li, AU - Cai,Yun-Lei, AU - Wang,Wen-Jing, AU - Wang,Wei-Ping, Y1 - 2016/03/03/ PY - 2015/12/12/received PY - 2016/02/23/revised PY - 2016/02/27/accepted PY - 2016/3/5/entrez PY - 2016/3/5/pubmed PY - 2016/8/23/medline KW - Kainic acid KW - Oxidative stress KW - Protection KW - Salidroside KW - Status epilepticus SP - 19 EP - 24 JF - Neuroscience letters JO - Neurosci Lett VL - 618 N2 - 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. SN - 1872-7972 UR - https://www.unboundmedicine.com/medline/citation/26940236/Salidroside_protects_against_kainic_acid_induced_status_epilepticus_via_suppressing_oxidative_stress_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(16)30122-7 DB - PRIME DP - Unbound Medicine ER -