Neuroprotective Effect of Ginsenoside Rd in Spinal Cord Injury Rats

Abstract

In this study, the neuroprotective effects of ginsenoside Rd (GS Rd) were evaluated in a rat model of spinal cord injury (SCI). Rats in SCI groups received a T8 laminectomy and a spinal contusion injury. GS Rd 12.5, 25 and 50 mg/kg were administered intraperitoneally 1 hr before the surgery and once daily for 14 days. Dexamethasone 1 mg/kg was administered as a positive control. Locomotor function was evaluated using the BBB score system. H&E staining and Nissl staining were performed to observe the histological changes in the spinal cord. The levels of MDA and GSH and the activity of SOD were assessed to reflect the oxidative stress state. The production of TNF-α, IL-1β and IL-1 was assessed using ELISA kits to examine the inflammatory responses in the spinal cord. TUNEL staining was used to detect the cell apoptosis in the spinal cord. Western blot analysis was used to examine the expression of apoptosis-associated proteins and MAPK proteins. The results demonstrated that GS Rd 25 and 50 mg/kg significantly improved the locomotor function of rats after SCI, reduced tissue injury and increased neuron survival in the spinal cord. Mechanically, GS Rd decreased MDA level, increased GSH level and SOD activity, reduced the production of pro-inflammatory cytokines and prevented cell apoptosis. The effects were equivalent to those of dexamethasone. In addition, GS Rd effectively inhibited the activation of MAPK signalling pathway induced by SCI, which might be involved in the protective effects of GS Rd against SCI. In conclusion, GS Rd attenuates SCI-induced secondary injury through reversing the redox-state imbalance, inhibiting the inflammatory response and apoptosis in the spinal cord tissue.

Protective effect of ginsenoside Rd against isoproterenolinduced myocardial infarction in Wistar rats

“…However, pretreatment with GRd reversed the ISO-induced increases in the levels of these inflammatory markers. These results are consistent with the results of Cong and Chen [11].…”

“…However, GRd treatment reversed the decreases in the activities of these cardiac antioxidants, while decreasing MDA. These results are in agreement with those reported in a previous study which also demonstrated that treatment with GRd considerably attenuated free radical generation by increasing the levels of SOD, and GSH [11]. Furthermore, it has been reported that treatment with GRd markedly upregulated the expression of nuclear factor-related factor 2 (Nrf2) and enhanced the production of SOD and glutathione [13].…”

“…Ginsenoside Rd (GRd) is the biologically active principle in Panax ginseng Radix or Chinese ginseng, a popular Chinese herb prescribed for various ailments of the cerebrovascular and cardiovascular system [9]. It is a steroid saponin with various pharmacological (antioxidant, antiinflammatory, anti-apoptotic and neuroprotective) properties [10,11]. Previous studies have demonstrated that GRd exerts protective effect against myocardial ischemic/reperfusion injury via modulation of Akt/GSK and Nrf2/HO-1 signalling pathways in various animal models [12,13].…”

Ginsenoside Rg3 Improves Recovery from Spinal Cord Injury in Rats via Suppression of Neuronal Apoptosis, Pro-Inflammatory Mediators, and Microglial Activation

“…Although ginsenosides, the main active ingredients in Panax ginseng C.A. Meyer, are not used to treat SCI regularly, their potential therapeutic effect in SCI treatment has been studied based on their anti-inflammatory, antioxidant, anti-apoptotic, and neuroprotective actions [ 7 , 8 , 9 , 10 , 11 ]. Crude extracts of ginseng improved the recovery of motor function after SCI by inhibiting post-traumatic inflammatory responses [ 7 , 8 ].…”

“…Ginsenoside Rb1 (GRb1) inhibited neuronal apoptosis and tissue damage by enhancing spinal aquaporin-4 expression and improved neurological deficits following spinal cord ischemia-reperfusion injury in rats [ 9 ]. Ginsenoside Rd (GRd) inhibited the activation of mitogen-activated protein kinase (MAPK) signaling pathway induced by SCI, and consequently improved the locomotor function of rats after SCI through its anti-inflammatory and anti-apoptotic actions [ 10 , 11 ].…”