Department of Anesthesiology, Shaanxi Provincial People's Hospital, Xi'an, China.
School of Life Sciences, Northwestern Polytechnical University, Xi'an, China.
Environ Toxicol. 2022 Dec;37(12):2889-2896. doi: 10.1002/tox.23645. Epub 2022 Aug 29.
Neuroinflammation contributes to the progression of cerebral ischemia/reperfusion (I/R) damage. Scutellarin (SL) is a glucuronide flavonoid that has apoptotic, anti-inflammatory, and anti-tumor properties. It is anti-oxidant and anti-inflammatory mechanism as a neuroprotective against ischemic brain injury is unknown. The purpose of the study was to examine the role and mechanism of SL in preventing I/R damage in a rat model. SL (40 and 80 mg/kg) was given to the rats for 14 days before the ischemic stroke. SL administration prevented I/R mediated brain injury, and neuronal apoptosis. Malondialdehyde, superoxide dismutase, glutathione, IL-6, and IL-1β and nitric oxide were modulated by SL. SL suppressed the p65 and p38 expressions in particular. The findings show that SL protects rats from cerebral damage caused by I/R through the nuclear factor kappa-B p65 and p38 mitogen-activated protein kinase signaling pathway. Thus, SL protected the brain of rats from ischemic injury by inhibiting the inflammatory process.
神经炎症会促进脑缺血/再灌注（I/R）损伤的进展。野黄芩苷（SL）是一种葡萄糖醛酸黄酮类化合物，具有促凋亡、抗炎和抗肿瘤的特性。其作为一种对抗缺血性脑损伤的神经保护剂的抗氧化和抗炎机制尚不清楚。本研究的目的是探讨 SL 在预防大鼠模型 I/R 损伤中的作用和机制。在缺血性脑卒中前，SL（40 和 80mg/kg）给大鼠给药 14 天。SL 给药可预防 I/R 介导的脑损伤和神经元凋亡。SL 调节丙二醛、超氧化物歧化酶、谷胱甘肽、IL-6、IL-1β 和一氧化氮。SL 特别抑制了 p65 和 p38 的表达。研究结果表明，SL 通过核因子 kappa-B p65 和丝裂原活化蛋白激酶 p38 信号通路来保护大鼠免受 I/R 引起的脑损伤。因此，SL 通过抑制炎症过程来保护大鼠的大脑免受缺血性损伤。
