Iranian journal of basic medical sciences · 2026
Sappanone A suppresses CHOP expression and exerts neuroprotective effects in epilepsy.
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Fu Jie, Li Jinglun, Chen Xiu
Аннотация
OBJECTIVES: Sappanone A (SA) is a compound derived from Caesalpinia sappan L that exhibits multiple biological effects, including anti-apoptotic, anti-inflammatory, and anti-oxidant activities. Because oxidative stress, cell apoptosis, and neuroinflammation are associated with the pathophysiology of epilepsy, we conducted this study to explore the role of SA in epilepsy.
MATERIALS AND METHODS: We used SA to treat pentylenetetrazole (PTZ)-induced mice as well as HT22 hippocampal cells exposed to Mg²⁺-free solution. Seizure behavior in the mice was recorded. Nissl staining, TUNEL assay, and flow cytometry were used to evaluate neuronal damage and apoptosis. Moreover, we employed biochemical tests to assess inflammation and oxidative stress levels, and conducted quantitative reverse transcription polymerase chain reaction and western blot to detect CHOP expression.
RESULTS: Pretreatments with SA (25 and 50 mg/kg) significantly prolonged seizure latency and reduced seizure duration in PTZ-induced epileptic mice (all P<0.001), whereas 10 mg/kg had no significant effects. At effective doses, SA also alleviated neuronal damage, reduced inflammation, and attenuated oxidative stress (all P<0.05). Furthermore, SA suppressed CHOP expression, and CHOP overexpression partially reversed SA's protective effects (P<0.05).
CONCLUSION: Our findings suggest that SA pretreatment exerts neuroprotective effects against epilepsy, potentially through suppression of CHOP expression. However, the causal relationship between CHOP suppression and SA-mediated neuroprotection in epilepsy warrants further investigation.
MATERIALS AND METHODS: We used SA to treat pentylenetetrazole (PTZ)-induced mice as well as HT22 hippocampal cells exposed to Mg²⁺-free solution. Seizure behavior in the mice was recorded. Nissl staining, TUNEL assay, and flow cytometry were used to evaluate neuronal damage and apoptosis. Moreover, we employed biochemical tests to assess inflammation and oxidative stress levels, and conducted quantitative reverse transcription polymerase chain reaction and western blot to detect CHOP expression.
RESULTS: Pretreatments with SA (25 and 50 mg/kg) significantly prolonged seizure latency and reduced seizure duration in PTZ-induced epileptic mice (all P<0.001), whereas 10 mg/kg had no significant effects. At effective doses, SA also alleviated neuronal damage, reduced inflammation, and attenuated oxidative stress (all P<0.05). Furthermore, SA suppressed CHOP expression, and CHOP overexpression partially reversed SA's protective effects (P<0.05).
CONCLUSION: Our findings suggest that SA pretreatment exerts neuroprotective effects against epilepsy, potentially through suppression of CHOP expression. However, the causal relationship between CHOP suppression and SA-mediated neuroprotection in epilepsy warrants further investigation.