Kafkas Universitesi Veteriner Fakültesi Dergisi (Aug 2022)

Cerebroprotective effects of yizhitongmai granule and decomposed recipes on vascular dementia rats via the nod-like receptor protein 3 infl ammasome pathway

  • Min PENG,
  • Guomin SI,
  • Hongbo MA,
  • Yuan LIU,
  • Qianqian LIU,
  • Hongyan MENG

DOI
https://doi.org/10.9775/kvfd.2022.27531
Journal volume & issue
Vol. 28, no. 5
pp. 553 – 560

Abstract

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We aimed to evaluate the cerebroprotective eff ects of Yizhitongmai Granule and its decomposed recipes on vascular dementia (VD) rats via the Nod-like receptor protein 3 (NLRP3) infl ammasome pathway. Sixty rats were randomly divided into Sham, VD Model, Yizhitongmai Recipe, Bushen Recipe, Tongluo Recipe and positive control groups (n=10). From 12 d aft er operation, Yizhitongmai Recipe, Bushen Recipe and Tongluo Recipe groups were gavaged with corresponding drug liquid. Th e drugs were administered at 2 mL once a day for 28 consecutive days. Th e reactive oxygen species (ROS), superoxide dismutase (SOD), total antioxidant capacity (T-AOC) and lactate dehydrogenase (LDH) in hippocampal tissues were detected using biochemical methods. Tumor necrosis factor-α (TNF-α), interleukin-18 (IL-18) and IL-1β were detected by enzyme-linked immunosorbent assay. Western blotting was performed to detect the expression levels of neuronal growth-associated protein-43 (GAP43), synaptophysin (SYN), aquaporin 4 (AQP4), NLRP3 and Caspase-1. Compared with the Model group, the number of apoptotic cells, levels of ROS, LDH, TNF-α, IL-18, IL-1β, NLRP3 and Caspase-1 decreased, and the levels of SOD, T-AOC, GAP43, SYN and AQP4 increased in the Yizhitongmai Recipe, Bushen Recipe and Tongluo Recipe groups (P0.05). Compared with the Bushen Recipe and Tongluo Recipe groups, the Yizhitongmai Recipe group had fewer apoptotic cells, decreased levels of ROS, LDH, TNF-α, IL-18, IL-1β, NLRP3 and Caspase-1, and increased levels of SOD, T-AOC, GAP43, SYN and AQP4 (P<0.05). Yizhitongmai Granule and its decomposed recipes can protect hippocampal neurons, relieve oxidative stress and infl ammatory response caused by hypoperfusion brain injury.

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