School of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, 21-1116 Xuzhou City, Jiangsu Province, PR China.
School of Life Science, Jiangsu Normal University, No.101, Shanghai Road, Tongshan New Area, 21-1116 Xuzhou City, Jiangsu Province, PR China.
Neurotoxicology. 2023 Sep;98:1-8. doi: 10.1016/j.neuro.2023.06.007. Epub 2023 Jun 28.
Lead (Pb) can cause neurobehavioral abnormalities. Isochlorogenic acid B (ICAB), a dietary flavonoid found in tea, sweet potato, artichoke, propolis and several plants, exhibited potential neuroprotective properties. In this study, we aimed to investigate the mechanisms of Pb-induced anxiety, depression and neuroinflammation, and the neuroprotective effect of ICAB in mouse brains. We found that ICAB supplementation significantly improved behavioral abnormalities, neuroinflammation and oxidative stress induced by Pb. ICAB attenuated Pb-induced anxiety and depression behavior in mice, as indicated by decreasing the duration of immobility in tail suspension test and increasing the crossing number, rearing number and time in center in open field test. Accordingly, ICAB inhibited oxidative stress by decreasing malondialdehyde (MDA) level and increasing the antioxidant enzyme activity. ICAB also inhibited Pb-induced inflammation in brain, as indicated by decreasing the tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels. ICAB increased the expression levels of brain derived neurotrophic factor (BDNF) and the phosphorylation of cAMP-responsive element binding protein (CREB), phosphoinositide 3-kinases-protein kinase B (PI3K/AKT). Furthermore, ICAB decreased the levels of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), glycogen synthase kinase-3 beta (GSK-3β) and p38. Collectively, this study demonstrated that ICAB improved Pb-induced anxiety, depression, neuroinflammation and oxidative stress by regulating the BDNF signaling pathway.
铅（Pb）可导致神经行为异常。异绿原酸 B（ICAB）是一种存在于茶、番薯、洋蓟、蜂胶和几种植物中的膳食类黄酮，具有潜在的神经保护作用。在本研究中，我们旨在探讨 Pb 诱导的焦虑、抑郁和神经炎症的机制，以及 ICAB 对小鼠大脑的神经保护作用。我们发现，ICAB 补充显著改善了 Pb 引起的行为异常、神经炎症和氧化应激。ICAB 减轻了 Pb 诱导的小鼠焦虑和抑郁行为，表现为悬尾试验中不动时间减少，旷场试验中穿越次数、站立次数和中央停留时间增加。因此，ICAB 通过降低丙二醛（MDA）水平和增加抗氧化酶活性来抑制氧化应激。ICAB 还抑制了脑内 Pb 诱导的炎症，表现为肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）水平降低。ICAB 增加了脑源性神经营养因子（BDNF）的表达水平和 cAMP 反应元件结合蛋白（CREB）、磷酸肌醇 3-激酶-蛋白激酶 B（PI3K/AKT）的磷酸化。此外，ICAB 降低了 Toll 样受体 4（TLR4）、髓样分化因子 88（MyD88）、糖原合成酶激酶-3β（GSK-3β）和 p38 的水平。综上所述，本研究表明，ICAB 通过调节 BDNF 信号通路改善了 Pb 诱导的焦虑、抑郁、神经炎症和氧化应激。
