Protective effect of geraniol inhibits inflammatory response, oxidative stress and apoptosis in traumatic injury of the spinal cord through modulation of NF-κB and p38 MAPK

Abstract

Abstract. Geraniol is a type of monoterpenoid with a rose scent and a slightly sweet flavor. It is found in the volatile oil of various plants, and has anti-inflammatory and anti-oxidant effects. The present study aimed to investigate the protective effect of geraniol in inhibiting the inflammatory response, oxidative stress and apoptosis in traumatic spinal cord injury (SCI), as well as to analyze the mechanism underlying its effect. Adult male Sprague-Dawley rats were induced to traumatic SCI through a surgical procedure and were defined as the SCI model group. SCI or normal rats were then administered 250 mg/kg/day geraniol for 4 weeks. The Basso, Beattie and Bresnahan (BBB) test and the spinal cord water content were used to analyze the effect of geraniol against traumatic SCI in rats. The inflammatory response, oxidative stress, and caspase-9 and -3 activities were measured using commercial ELISA kits. In addition, the associated mechanism was analyzed, using western blot analysis to determine the protein expression levels of nuclear factor (NF)-κB and p38 mitogen-activated protein kinase (MAPK). The results of the present study demonstrated that BBB scores were significantly increased and the spinal cord water content was significantly inhibited in SCI rats after 3 weeks of geraniol treatment. Furthermore, the inflammatory response, oxidative stress, and the caspase-9 and -3 activities were significantly suppressed upon treatment with geraniol. Finally, the mechanism of geraniol against traumatic SCI downregulated the NF-κB and p38 MAPK pathways in SCI rats. Therefore, the protective effect of geraniol is suggested to inhibit the inflammatory response, oxidative stress and apoptosis in traumatic SCI through the modulation of NF-κB and p38 MAPK.

Analysis of the Antioxidant Activity of Geraniol Employing Various in-Vitro Models: Relevance to Neurodegeneration in Diabetic Neuropathy

“…This includes their ability to reduce the levels of or the formation of ROS and RNS, concomitantly upregulating vitagenes, such as members of the heat shock protein (Hsp) family, heme oxygenase-1, and Hsp70 [8,26]. GE has been reported as an effective antioxidant and antiinflammatory agent in different experimental models from our lab and others [16][17][18][19]21,29]. Recently, the antioxidant activity of GE along with other actives has been published with respect to DPPH free radical scavenging activity and superoxide dismutase activity [30].…”

“…It is also found in a wide range of cleansing products and cosmetics for its appealing odor [13,14]. In the recent past, several studies have recognized the pharmacological potential of GE in different models [15][16][17]. Its pharmacological property is by virtue of its antioxidant and anti-inflammatory properties [18,19].…”

Geraniol alleviates LPS-induced acute lung injury in mice via inhibiting inflammation and apoptosis

“…GOH, a special type of acyclic monoterpene alcohol, has been widely used to treat many diseases related to inflammation, including dextran sulfate sodium (DSS)-induced colitis in mice [ 28 ]. Moreover, GOH has been shown to inhibit cell apoptosis in traumatic spinal cord injury (SCI) [ 29 ]. In our study, a mouse model of ALI was successfully established by the intranasal administration of LPS, and we investigated the anti-inflammatory and anti-apoptotic effects of GOH on LPS-induced ALI in mice.…”

Effects of apigenin on the expression levels of B‑cell lymphoma‑2, Fas and Fas ligand in renal ischemia‑reperfusion injury in rats

“…The Fas/FasL and Bcl-2 genes are two of the key factors influencing apoptosis and regulating the intrinsic apoptosis pathway in renal tubular epithelial cells ( 18 , 19 ). In addition, the intrinsic apoptosis pathway is activated by oxidative stress, which is mediated by increased mitochondrial membrane permeability ( 20 ). Previous studies have suggested that oxidative stress is involved in the apoptotic mechanism mediated by the Fas/FasL signaling pathway ( 21 – 23 ).…”