Protective effects of extract of Ginkgo biloba (EGb 761) on nerve cells after spinal cord injury in rats

Abstract

Study design: An experimental animal model was used to assess spinal cord injury following lateral hemitransection at thoracic spinal cord level. Objective: To determine whether extract of Ginkgo biloba (EGb) could have a neuroprotective effect in spinal cord injury (SCI) in rats. Setting: Department of Biological Sciences and Biotechnology, Tsinghua University, China. Methods: A total of 72 adult rats were divided randomly into three groups: the EGb group, normal saline (NS) group, and sham operation group (sham group). After thoracic spinal cord hemitransection was performed at the level of the 9th thoracic vertebra (T9), rats in the EGb group were given 100 mg/kg EGb 761 daily, while rats in the NS group received NS. The rats in the sham group only underwent laminectomy without spinal cord hemitransection. At various time points after surgery, thoracic spinal cords were sampled and sliced for histochemistry, immunohistochemistry of inducible nitric oxide synthase (iNOS), and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) of apoptotic cells. Results: Myelin staining showed that the area of cavities was small and the demyelinated zones were limited at and around the injury site of the spinal cord in the EGb group, while the area of cavities was large and the demyelinated zones were serious in the NS group. Nissl staining showed that the ratio of bilateral ventral horn neurons (transection side/uninjured side) in the EGb group was higher than that in the NS group (Po0.05). The apoptotic index and the percentage of iNOS-positive cells were lower in the EGb group than in the NS group. Furthermore, the percentage of iNOS-positive cells positively correlated with the apoptotic index (r 2 ¼ 0.729, Po0.01) after SCI. Conclusion: This study demonstrated that EGb 761 could inhibit iNOS expression and have neuroprotective effect by preventing nerve cells from apoptosis after SCI in rats.

Inhibition of cPLA2 activation by Ginkgo biloba extract protects spinal cord neurons from glutamate excitotoxicity and oxidative stress‐induced cell death

“…2009). Several in vivo experiments also showed that EGb761 protected spinal cord neurons after spinal ischemia‐reperfusion or injury (Ao et al. 2006; Mechirova et al.…”

“…This study shows that EGb761 protects spinal cord neurons from death induced by both injury insults in a dose-dependent manner, consistent with our previous report (Jiang et al 2009). Several in vivo experiments also showed that EGb761 protected spinal cord neurons after spinal ischemia-reperfusion or injury (Ao et al 2006;Mechirova et al 2009). EGb761 was also shown to reduce neuronal death in global brain ischemia and Glu-induced excitotoxicity (Chandrasekaran et al 2002), and inhibit NMDA receptor-mediated calcium influx and neuronal death (Szasz et al 2008;Shi et al 2010).…”

Antiapoptotic Effects of EGb 761

“…In addition, in lymphocytes isolated from spleen of aged mice treated with 100 mg/Kg EGb 761 for 2 weeks, less susceptibility to ROS-induced apoptosis was found [45]. In the peripheral nervous system, posttreatment with EGb 761 (100 mg/kg) decreased the number of apoptotic cells in injured rat spinal cord [46]. In central nervous system, treatment with EGb 761 (40 mg/kg) reduced neuronal death in the substantia nigra pars compacta from an experimental model of Parkinson's disease [47].…”

Extract of Ginkgo biloba exacerbates liver metastasis in a mouse colon cancer Xenograft model

“…Furthermore, it has been reported that EGb has anticancer effects in breast and gallbladder cancers [ 11 , 12 ]. These effects potentially involve diverse mechanisms, including the reduction in the number of apoptotic cells [ 13 – 16 ], the maintenance of mitochondrial integrity [ 17 – 20 ], inhibition of cyt c release from mitochondria, induction of gene expression of the anti-apoptotic protein Bcl-2 [ 21 – 25 ], reduction in the gene expression of caspases [ 21 , 24 , 26 – 28 ] and DNA fragmentation [ 21 , 24 ]. In addition, EGb up-regulates the mRNA expression of antioxidant enzymes such as mitochondrial SOD, GPx, GCLC, and HO-1 to decrease oxidative tissue damage [ 29 – 31 ].…”