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Updated: Feb 7, 2026
Anteromesial Temporal Lobectomy for Medically Intractable Temporal Lobe Epilepsy: An Operative Study
Published on: August 15, 2025
Correlation between tumor necrosis factor alpha mRNA and microRNA-155 expression in rat models and patients with
Tao-Ran Li1, Yan-Jie Jia2, Qun Wang3
1Department of Neurology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang Medical University, 88 Road of JianKang, WeiHui, Xinxiang 453100, PR China; Department of Neurology, Beijing Tiantan Hospital, Capital Medical University; China National Clinical Research Center for Neurological Diseases, 6 TianTanXiLi, Dongcheng District, Beijing 100050, PR China.
Abstract:
Accumulative evidence demonstrates that there is an inseparable connection between inflammation and temporal lobe epilepsy (TLE). Some recent studies have found that the multifunctional microRNA-155 (miR-155) is a key regulator in controlling the neuroinflammatory response of TLE rodent animals and patients. The aim of the present study was to investigate the dynamic expression pattern of tumor necrosis factor alpha (TNF-α) as a pro-inflammatory cytokine and miR-155 as a posttranscriptional inflammation-related miRNA in the hippocampus of TLE rat models and patients. We performed real-time quantitative PCR (qRT-PCR) on the rat hippocampus 2 h, 7 days, 21 days and 60 days following kainic acid-induced status epilepticus (SE) and on hippocampi obtained from TLE patients and normal controls. To further characterize the relationship between TNF-α and miR-155, we examined the effect of antagonizing miR-155 on TNF-α secretion using its antagomir. Here, we found that TNF-α secretion and miR-155 expression levels were correlated after SE. The expression of TNF-α reached peak levels in the acute phase (2h post-SE) of seizure and then gradually decreased; however, it rose again in the chronic phase (60 days post-SE). miR-155 expression started to increase 2 h post-SE, reached peak levels in the latent phase (7 days post-SE) of seizure and then gradually decreased. The variation in the trend of miR-155 lagged behind that of TNF-α. In patients with TLE, the expression levels of both TNF-α and miR-155 were also significantly increased. Furthermore, antagonizing miR-155 inhibited the production of TNF-α in the hippocampal tissues of TLE rat models. Our findings demonstrate a critical role for miR-155 in the physiological regulation of the TNF-α pro-inflammatory response and elucidate the role of neuroinflammation in the pathogenesis of TLE. Therefore, regulation of the miR-155/TNF-α axis may be a new therapeutic target for TLE.
Insights
Neuroinflammation and temporal lobe epilepsy (TLE) are linked, with microRNA-155 (miR-155) regulating this response. This study shows miR-155 and tumor necrosis factor alpha (TNF-α) are elevated in TLE, and targeting miR-155 reduces TNF-α, suggesting a new therapeutic approach.
Area of Science:
- Neuroscience
- Molecular Biology
- Pathology
Background:
- Inflammation is closely linked to temporal lobe epilepsy (TLE).
- MicroRNA-155 (miR-155) is identified as a key regulator of neuroinflammation in TLE.
- Tumor necrosis factor alpha (TNF-α) is a significant pro-inflammatory cytokine implicated in TLE.
Purpose of the Study:
- To investigate the dynamic expression patterns of TNF-α and miR-155 in the hippocampus of TLE rat models and patients.
- To characterize the relationship between TNF-α and miR-155 expression following seizures.
- To explore the therapeutic potential of targeting the miR-155/TNF-α axis in TLE.
Main Methods:
- Real-time quantitative PCR (qRT-PCR) was used to measure TNF-α and miR-155 expression in rat hippocampi at various time points post-status epilepticus (SE) and in human TLE samples.
- Antagomirs were employed to inhibit miR-155 function and assess its effect on TNF-α secretion.
- Hippocampal tissues from TLE patients and normal controls were analyzed.
Main Results:
- TNF-α expression peaked in the acute phase and chronic phase post-SE, while miR-155 expression peaked in the latent phase, with miR-155 trends lagging behind TNF-α.
- Both TNF-α and miR-155 levels were significantly elevated in the hippocampi of TLE patients compared to controls.
- Inhibition of miR-155 using antagomirs led to a reduction in TNF-α production in TLE rat models.
Conclusions:
- miR-155 plays a critical role in the physiological regulation of the pro-inflammatory cytokine TNF-α.
- Neuroinflammation, mediated by the miR-155/TNF-α pathway, is implicated in the pathogenesis of TLE.
- Targeting the miR-155/TNF-α axis represents a potential novel therapeutic strategy for TLE.
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