Jiaohong pills attenuate neuroinflammation and amyloid-β protein-induced cognitive deficits by modulating the mitogen-activated protein kinase/nuclear factor kappa-B pathway

焦红丸通过调节丝裂原活化蛋白激酶/核因子 κB 通路减轻神经炎症和淀粉样β蛋白引起的认知障碍

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作者:Hong Zhang, Weiyan Cai, Lijinchuan Dong, Qing Yang, Qi Li, Qingsen Ran, Li Liu, Yajie Wang, Yujie Li, Xiaogang Weng, Xiaoxin Zhu, Ying Chen

Background

Jiaohong pills (JHP) consist of Pericarpium Zanthoxyli (PZ) and Radix Rehmanniae, two herbs that have been extensively investigated over many years due to their potential protective effects against cognitive decline and memory impairment. However, the precise mechanisms underlying the beneficial effects remain elusive. Here, research studies were conducted to investigate and validate the therapeutic effects of JHP on Alzheimer's disease.

Conclusions

It was found that JHP reduced neuroinflammatory response in AD mice by targeting the MAPK/NF-κB signaling pathway.

Methods

BV-2 cell inflammation was induced by lipopolysaccharide. AD mice were administered amyloid-β (Aβ). Behavioral experiments were used to evaluate learning and memory ability. The levels of nitric oxide (NO), tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-10 (IL-10) were detected using enzyme-linked immunosorbent assay (ELISA). The protein expressions of inducible nitric oxide synthase (iNOS) and the phosphorylation level of mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) were detected using Western blot. Nissl staining was used to detect neuronal degeneration.

Results

The results demonstrated that an alcoholic extract of PZ significantly decreased the levels of NO, IL-1β, TNF-α, and iNOS; increased the expression level of IL-10; and significantly decreased the phosphorylation levels of MAPK and NF-κB. These inhibitory effects were further confirmed in the AD mouse model. Meanwhile, JHP improved learning and memory function in AD mice, reduced neuronal damage, and enriched the Nissl bodies in the hippocampus. Moreover, IL-1β and TNF-α in the cortex were significantly downregulated after JHP administration, whereas IL-10 showed increased expression. Conclusions: It was found that JHP reduced neuroinflammatory response in AD mice by targeting the MAPK/NF-κB signaling pathway.

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