Curcumin protects neuronal cells against status-epilepticus-induced hippocampal damage through induction of autophagy and inhibition of necroptosis.
Status epilepticus, the most severe form of epilepsy, is characterized by progressive functional and structural damage in the hippocampus, ultimately leading to the development and clinical appearance of spontaneous, recurrent seizures. Although the pathogenesis underlying epileptogenesis processes remains unclear, a substantial body of evidence has shown that status epilepticus acts as an important initial factor in triggering epileptogenesis. Notably, besides classical cell death mechanisms such as apoptosis and necrosis, 2 novel regulators of cell fate known as necroptosis and autophagy, are demonstrated to be involved in neuronal damage in various neurodegenerative and neuropsychiatric disorders. However, whether necroptosis and autophagy play a role in post-status-epilepticus rat hippocampus and other epilepsy mechanisms deserves further research effort. In addition, research is needed to determine whether compounds from traditional Chinese herbs possess antiepileptic effects through the modulation of necroptosis and autophagy. In this study, we found that curcumin, a polyphenolic phytochemical extracted from the Curcuma longa plant, protects neuronal cells against status-epilepticus-induced hippocampal neuronal damage in the lithium-pilocarpine-induced status epilepticus rat model through induction of autophagy and inhibition of necroptosis.
a Department of Pharmacology, Xiangya School of Medicine, Central South University, Changsha 410008, China.
Jin
J
Wang
b Department of Anesthesia, Xiangya School of Medicine, Central South University, Changsha 410008, China.
Yuan
Y
Liu
a Department of Pharmacology, Xiangya School of Medicine, Central South University, Changsha 410008, China.
Xiao-Hui
XH
Li
c Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha 410008, China.|d Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University, Changsha 410078, China.
Xiang-Chang
XC
Zeng
e Department of Laboratory Medicine, Xiangya School of Medicine, Central South University, Changsha 410008, China.
Jian
J
Li
f Medical Science Research Center, Xiangya Hospital, Central South University, Changsha 410008, China.
Jun
J
Zhou
g Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China.
Bo
B
Xiao
g Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China.
Kai
K
Hu
D000818:Animals; D001343:Autophagy / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D003474:Curcumin / Q000494:pharmacology* / Q000627:therapeutic use; D019610:Cytoprotection / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology*; D008297:Male; D009336:Necrosis; D009474:Neurons / Q000187:drug effects* / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000188:drug therapy / Q000473:pathology*
D003474:Curcumin
autophagie; autophagy; curcumin; curcumine; hippocampe; hippocampus; necroptosis; nécroptose; status epilepticus; état de mal épileptique