P38 MAPK pathway mediates cognitive damage in pentylenetetrazole-induced epilepsy via apoptosis cascade

Huang, Qi; Liu, Xixia; Wu, Yuan; Liao, Yuhan; Huang, Yiqing; Wei, Xing; Ma, Meigang

doi:10.1016/j.eplepsyres.2017.04.012

Cited by 23 publications

(16 citation statements)

References 36 publications

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“…The retrieval memory impairment accompanied by PTZ chronic treatment was previously demonstrated in numerous previous studies in elevated plus maze (EPM) paradigm [2,33,[41][42][43] and several other behavioral tests, e.g., MWM paradigm [44][45][46]. In the current study, the procognitive effect of H3R antagonist E177 (5 and 10 mg/kg, i.p.)…”

Section: Effects Of E177 On Mmemory Deficits In Inhibitory Avoidance supporting

confidence: 58%

Antagonism of Histamine H3 receptors Alleviates Pentylenetetrazole-Induced Kindling and Associated Memory Deficits by Mitigating Oxidative Stress, Central Neurotransmitters, and c-Fos Protein Expression in Rats

et al. 2020

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Histamine H3 receptors (H3Rs) are involved in several neuropsychiatric diseases including epilepsy. Therefore, the effects of H3R antagonist E177 (5 and 10 mg/kg, intraperitoneal (i.p.)) were evaluated on the course of kindling development, kindling-induced memory deficit, oxidative stress levels (glutathione (GSH), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD)), various brain neurotransmitters (histamine (HA), acetylcholine (ACh), γ-aminobutyric acid (GABA)), and glutamate (GLU), acetylcholine esterase (AChE) activity, and c-Fos protein expression in pentylenetetrazole (PTZ, 40 mg/kg) kindled rats. E177 (5 and 10 mg/kg, i.p.) significantly decreased seizure score, increased step-through latency (STL) time in inhibitory avoidance paradigm, and decreased transfer latency time (TLT) in elevated plus maze (all P < 0.05). Moreover, E177 mitigated oxidative stress by significantly increasing GSH, CAT, and SOD, and decreasing the abnormal level of MDA (all P < 0.05). Furthermore, E177 attenuated elevated levels of hippocampal AChE, GLU, and c-Fos protein expression, whereas the decreased hippocampal levels of HA and ACh were modulated in PTZ-kindled animals (all P < 0.05). The findings suggest the potential of H3R antagonist E177 as adjuvant to antiepileptic drugs with an added advantage of preventing cognitive impairment, highlighting the H3Rs as a potential target for the therapeutic management of epilepsy with accompanied memory deficits.

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Section: Effects Of E177 On Mmemory Deficits In Inhibitory Avoidance supporting

confidence: 58%

Antagonism of Histamine H3 receptors Alleviates Pentylenetetrazole-Induced Kindling and Associated Memory Deficits by Mitigating Oxidative Stress, Central Neurotransmitters, and c-Fos Protein Expression in Rats

et al. 2020

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“…To further explore the interaction between miR-181b and TLR4, as well as its underlying mechanism in epilepsy, we gave an injection of miR-181b agomir or TAK-242 (TLR4 inhibitor) to KAinduced epileptic juvenile rats, and our findings demonstrated that the spatial memory abilities of rats, as a kind of advanced neural activity of brain, which was an important element of both cognition and intelligence structure, whereas many epileptic patients have severe cognitive impairment, were significantly improved. 36 While apoptosis, as a critical programmed cell death, exerts vital effects on hippocampal neuron injury postseizure, 39 and inhibition of apoptosis has important neuro-protective effects on hippocampal neuronal injury postseizure. 40,41 Currently, growing evidence supported that neuronal apoptosis can lead to upregulation of proapoptotic protein Bax and downregulation of antiapoptotic proteinBcl-2 after SE seizure.…”

Section: Discussionmentioning

confidence: 99%

MiR‐181b inhibits P38/JNK signaling pathway to attenuate autophagy and apoptosis in juvenile rats with kainic acid‐induced epilepsy via targeting TLR4

et al. 2018

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“…The results showed that RHL‐induced cell apoptosis was not mediated by the activation of JNK in spinal cord tissues after SCI. In various systems, the proapoptotic/growth inhibitory effects of p38 MAPK has been reported . The results showed that the positive expression of p38 MAPK in the SCI group was significantly higher than that in the sham operation group, indicating growth inhibition in spinal cord tissues.…”

Section: Resultsmentioning

confidence: 99%

Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

Hao

Wang

Daiping

et al. 2019

The Kaohsiung J of Med Scie

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The current study aims to investigate the effect of rhein lysinate (RHL) on neuromotor function in rats with spinal cord injury (SCI) and to explore the underlying mechanism. A total of 63 adult male SD rats were randomly divided into the sham group, SCI group and RHL group (SCI‐RHL group), with 21 rats in each group. Basso Beattie Bresnahan (BBB) scoring and the inclined plate test were used to evaluate the changes in motor function after SCI. Then, superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and malondialdehyde (MDA) contents were quantified. Caspase‐3‐positive cells in spinal cord tissue were detected by immunohistochemical (IHC) staining, and protein expression was detected by Western blots. Here, our data showed that compared with the SCI group, the BBB score and inclined plate test score of the SCI‐RHL group were significantly higher than those of the SCI group 7 days after the RHL intervention. After 7 days of RHL treatment, the activities of SOD and GSH‐Px in the spinal cord increased significantly. At the same time, RHL reduced the MDA content in spinal cord tissue of SCI rats. Moreover, cleaved‐caspase‐3‐positive cells and apoptotic cells were significantly lower in the SCI‐RHL group than in the SCI group. More importantly, p38 mitogen‐activated protein kinase (p38 MAPK) was significantly decreased in the SCI‐RHL group compared with the SCI group. In summary, RHL can inhibit the activation of the p38 MAPK pathway after SCI, thereby reducing the apoptosis of spinal cord neurons and improving the neuromotor function of SCI rats.

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P38 MAPK pathway mediates cognitive damage in pentylenetetrazole-induced epilepsy via apoptosis cascade

Cited by 23 publications

References 36 publications

Antagonism of Histamine H3 receptors Alleviates Pentylenetetrazole-Induced Kindling and Associated Memory Deficits by Mitigating Oxidative Stress, Central Neurotransmitters, and c-Fos Protein Expression in Rats

Antagonism of Histamine H3 receptors Alleviates Pentylenetetrazole-Induced Kindling and Associated Memory Deficits by Mitigating Oxidative Stress, Central Neurotransmitters, and c-Fos Protein Expression in Rats

MiR‐181b inhibits P38/JNK signaling pathway to attenuate autophagy and apoptosis in juvenile rats with kainic acid‐induced epilepsy via targeting TLR4

Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

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