Gastrodin ameliorates spinal cord injury via antioxidant and anti-inflammatory effects

Abstract

Spinal cord injury (SCI) is one of the most severe traumatic injuries that results in dysfunction of limbs and trunk below the damaged section. Recent studies have shown that gastrodin (GAS) could improve the recovery of SCI. In the current study, we aimed to examine the possible mechanism underlying the effect of GAS on recovery of SCI in rats. In rats with SCI, GAS improved locomotor functions and decreased permeability of blood-spinal cord barrier, as illustrated by increase of Basso-Beattie-Bresnahan scores and decrease of Evans blue leakage. In addition, GAS inhibited inflammation, as evidenced by decrease of proinflammatory cytokines, including tumor necrosis factor α (TNFα) and interleukin-1β (IL-1β) in rats following SCI. Moreover, increase of TBARS content and decrease of glutathione (GSH) content and superoxide dismutase (SOD) activities in SCI rats were inhibited by GAS. Furthermore, GAS enhanced mRNA expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), catalytic subunit of γ-glutamylcysteine ligase (GCLc) and modified subunit of γ-glutamylcysteine ligase (GCLm). The data suggested that GAS may promote the recovery of SCI through the enhancement of Nrf2-GCLc/GCLm signaling pathway, and subsequent improvement of oxidative stress and inflammation, resulting in decrease of permeability of BSCB and improved recovery of locomotor function in rats with SCI. The results have provided novel insights into GAS-related therapy of SCI and associated neurodegenerative diseases.

Silver nanoparticle-induced expression of proteins related to oxidative stress and neurodegeneration in an in vitro human blood-brain barrier model

“…The late response of the endothelial cells was characterized by the production of various antioxidant proteins (Figure 7). It is known that antioxidants proteins have beneficial effects on the BBB damage responses and play a major role in its recovery from damage (Du et al 2016;Janyou et al 2017;Jumnongprakhon et al 2015;Lim et al 2016;Mendes Arent et al 2014;Benvenisti-Zarom and Regan 2007). Antioxidant proteins like nuclear factor-like 2 protein (Nrf2) and heme oxygenase-1 (HMOX-1) have been defined as oxidative-sensor proteins.…”

“…The antioxidant proteins were significantly upregulated after 48 h AgNPs exposure compared to its expression at 24 h exposure. The anti-oxidant proteins NQO1 and GCLM are also reported to be involved in endogenous cellular stress responses and to protect cells from ROS-induced damage and cell death (Du et al 2016;Lin et al 2017;Zhang, Davies, and Forman 2015). Thus, increased production of these proteins after AgNPs exposure may indicate the activation of various oxidative and inflammatory injury response cascades in response to AgNPs., NQO1 expression was elevated after 48 h AgNPs exposure.…”

Gastrodin alleviates bone damage by modulating protein expression and tissue redox state

“…Elevated levels of Bcl-2 and a decrease in Bax indicate that cells are more resistant to apoptosis and should be a marker of protective drug action, and vice versa. Studies have found that oxidative stress caused by high doses of NaF leads to mitochondrial damage, leading to osteogenic and osteoclast apoptosis [32,36]. The caspase cascade is triggered by caspase-9, after which caspase-3 becomes activated by caspase-9.…”

Identification and Investigation of miRNAs From Gastrodia elata Blume and Their Potential Function

“…In ancient China, G. elata was widely used to treat headache, dizziness, paralysis, epilepsy, joint pain, and numbness of limbs ( Zhan et al., 2016 ). Some studies on its pharmacological properties have shown that G. elata has neuroprotective and antioxidant functions and could be used as an anti-inflammatory and antipsychotic drug ( Kumar et al., 2013 ; Hu et al., 2014 ; Du et al., 2016 ; Wang et al., 2016 ). The pharmacological mechanisms of potential anticonvulsant activity of arrow G. elata have been extensively studied, which is similar to the mechanisms of known antiepileptic drugs ( Wu et al., 2017 ).…”