Ginsenoside RK1 inhibits microglial activation and ROS production and alleviates vascular dementia in rats.

Although ginsenoside RK1 (RK1) possesses neuroprotective properties, it is unknown how it relates to vascular dementia (VD). The purpose of this work was to show that RK1 has a neuroprotective function in VD. First, the VD rat model was established by ligating the carotid artery with two-vessel occlusion (2-VO) surgery. RK1 was given daily for 30 days. A water maze test evaluated the learning and memory functions of the rats in each group. HE staining was used to assess the pathological damage of hippocampal tissue. The microglial marker Iba-1, proinflammatory factors [tumor necrosis factor alpha (TNF-α), Interleukin (IL)-1β, and IL-6], reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and peroxisome proliferator-activated receptor γ (PPARγ) in the hippocampal tissue were detected. The results show that RK1 reduced the escape latency of VD rats, increased the time VD rats stayed in the target quadrant and the number of times they crossed the platform, and alleviated the pathological damage of hippocampal tissue. In addition, RK1 also inhibited the activation of microglia and ROS production in the hippocampus of VD rats, reduced the content of proinflammatory factors and MDA, increased the content of antioxidant enzyme SOD, and activated PPARγ expression in hippocampal tissue. Overall, RK1 alleviates cognitive dysfunction and hippocampal tissue pathological damage in VD rats and inhibits hippocampal neuroinflammation and ROS production, which may be related to the activation of PPARγ in hippocampal tissue by RK1.