Department of Pediatrics, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University, Fuzhou University Affiliated Provincial Hospital, Fuzhou, Fujian Province, China, 350001.
Department of Pediatrics, Fujian Provincial Hospital, Provincial Clinical Medical College of Fujian Medical University, 134 East Street, Gulou District, Fuzhou, Fujian Province, China, 350001.
Metab Brain Dis. 2024 Oct;39(7):1387-1403. doi: 10.1007/s11011-024-01401-z. Epub 2024 Sep 18.
The study examined curcumin's impart on relieving neuroinflammation of juvenile rats in kainic acid (KA) induced epileptic seizures by inhibiting the TLR4/MyD88/NF-κB pathway. There were five groups: control, KA, KA + curcumin (KC), KA + oxcarbazepine (OXC) (KO), KA + curcumin + OXC (KCO) groups. KA was stereotactically injected into right hippocampus following intraperitoneal injection of curcumin or (and) OXC for seven days. The rats in the above groups were randomly divided into three subgroups (at 6 h, 24 h, and 72 h of KA administration) following the seizure degree assessed. The number of NeuN (+) neurons and GFAP (+) astrocytes was counted. The gene and protein levels of TLR4, MyD88, and NF-κB were detected. Compared with the KA group, the seizure latency was longer, and the incidence of status epilepticus (SE) was lower in the KC, KO, and KCO groups. The most significant changes were in the KCO group. At 72 h following KA injected, the number of neurons was the least, and the number of astrocytes was the most in the KA group. The number of neurons was the most and the number of astrocytes was the least in the KCO group. At 24 h, the mRNA and protein levels of TLR4, MyD88, and NF-κB in the KA group were the most. The above valves were the least in the KCO group. Therefore, curcumin could enhance anti-epileptic effect of OXC, protect injured neurons and reduce proliferated glial cells of the hippocampus of epileptic rats by inhibiting inflammation via the TLR4/MyD88/NF-κB pathway.
该研究通过抑制 TLR4/MyD88/NF-κB 通路，考察姜黄素对海人酸（KA）诱导的癫痫发作中幼年大鼠神经炎症的缓解作用。共分为五组：对照组、KA 组、KA+姜黄素（KC）组、KA+奥卡西平（OXC）组（KO）、KA+姜黄素+奥卡西平组（KCO）。KA 经腹腔注射后，立体定向注射入右侧海马，7 天内给予姜黄素和（或）奥卡西平。上述各组大鼠根据癫痫发作程度分为三组（KA 给药后 6、24 和 72 h）。计数 NeuN（+）神经元和 GFAP（+）星形胶质细胞数量。检测 TLR4、MyD88 和 NF-κB 的基因和蛋白水平。与 KA 组相比，KC、KO 和 KCO 组的癫痫潜伏期延长，癫痫持续状态（SE）发生率降低，其中 KCO 组变化最明显。KA 注射后 72 h，KA 组神经元数量最少，星形胶质细胞数量最多。KCO 组神经元数量最多，星形胶质细胞数量最少。24 h 时，KA 组 TLR4、MyD88 和 NF-κB 的 mRNA 和蛋白水平最高，KCO 组上述值最低。因此，姜黄素可通过 TLR4/MyD88/NF-κB 通路抑制炎症，增强 OXC 的抗癫痫作用，保护癫痫大鼠海马受损神经元，减少胶质细胞增生。
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