Increased neuronal seizure activity correlates with excessive systemic inflammation in a rat model of severe preeclampsia.
Preeclampsia (PE), one of the most common disorders of pregnancy, is characterized by hypertension and albuminuria. In severe cases, PE results in eclampsia-like seizures. Studies have suggested that severe PE is related to an exaggerated systemic inflammatory response, which may increase sensitivity to seizures. In the current study, we investigated whether the seizure activity of neurons was enhanced under excessive systemic inflammation. We also sought to determine whether MgSO4could reduce the effects of systemic inflammation on seizure activity after electrical stimulation in a lipopolysaccharide (LPS)-induced model of PE. In addition to pregnancy outcomes, we analyzed biochemical parameters to ascertain whether our PE model was successful. Enzyme-linked immunosorbent assay analysis revealed that the levels of inflammatory cytokines (tumor necrosis factor (TNF)-α and interleukin (IL)-1β) were significantly higher in the LPS-treated rats than in the untreated rats. After electrical stimulation, behavioral assessments showed that the LPS-treated rats that were not treated with MgSO4had the shortest latency period to develop a seizure and the longest seizure duration. The electroencephalographic (EEG) recordings in the hippocampus demonstrated that this group also had the highest EEG amplitude. MgSO4treatment significantly decreased both TNF-α and IL-1β concentrations, increased the latency to develop a seizure, decreased the seizure duration and shortened the EEG amplitude. These results suggest that neuronal seizure activity and systemic inflammation are increased in severe PE. In addition, MgSO4treatment reduced systemic inflammation and seizure severity. We conclude that excessive systemic inflammation in PE promotes eclampsia seizures, which can be attenuated by MgSO4treatment.
Department of Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou medical University, Guangzhou, China.
Lei
L
Liu
Department of Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou medical University, Guangzhou, China.
Xinjia
X
Han
Department of Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou medical University, Guangzhou, China.
Qian
Q
Huang
Department of Physiology, Guangzhou medical University, Guangzhou, China.
Xiaoqin
X
Zhu
Department of Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou medical University, Guangzhou, China.
Jinying
J
Yang
Department of Obstetrics, Guangzhou Women and Children's Medical Center, Guangzhou medical University, Guangzhou, China.
Huishu
H
Liu
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004569:Electroencephalography; D005260:Female; D006624:Hippocampus / Q000503:physiopathology; D007249:Inflammation / Q000097:blood / Q000503:physiopathology*; D053583:Interleukin-1beta / Q000097:blood; D008278:Magnesium Sulfate / Q000494:pharmacology / Q000627:therapeutic use*; D009474:Neurons / Q000502:physiology*; D011225:Pre-Eclampsia / Q000097:blood / Q000503:physiopathology*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D000927:Anticonvulsants; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D008278:Magnesium Sulfate