Hesperidin improves motor disability in rat spinal cord injury through anti-inflammatory and antioxidant mechanism via Nrf-2/HO-1 pathway. (10th January 2020)

• Record Type: Journal Article
• Authors: Heo, Seung-Dam; Kim, Jeongtae; Choi, Yuna; Ekanayake, Poornima; Ahn, Meejung; Shin, Taekyun
• Is Part Of: Neuroscience letters. Volume 715(2020)
• Publication Date: 2020-01-10
• Subjects: Spinal cord injury -- Hesperidin -- Motor disability -- Heme oxygenase-1; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2019.134619
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Hesperidin ameliorated SCI-induced hindlimb paralysis in rats. Hesperidin regulated pro-inflammatory mediators and oxidative stress. Hesperidin enhanced bilirubin and Fe 2+ in the serum of SCI rats. Hesperidin activated Nrf-2/HO-1 pathway in the SCI lesions. Abstract: Spinal cord injury (SCI) is associated with inflammation with concurrent oxidative stress and glial activation. The aim of this study was to evaluate whether hesperidin, a representative flavonoid in citrus fruits, ameliorates SCI-induced motor dysfunction and neuro-pathologic degeneration in rat model. Rats received hesperidin (100 mg/kg body weight/daily, oral administration) from 7 days prior to SCI to 7 days post SCI. Behavioral test was done on rats with SCI until 6 weeks. For the study of inflammatory molecules in SCI rats with hesperidin treatment, rats were sacrificed at day 4 post SCI, and spinal cords were collected and studied histopathologically. Behavioral tests on hind-limbs of rats with SCI revealed that treatment of hesperidin in rats with SCI significantly ameliorate the hind-limb paralysis beginning at day 21 post SCI. Hesperidin treatment in rats with SCI reduced the neuropathological changes (e.g., hemorrhage, inflammatory cell infiltration, and tissue loss) and pro-inflammatory cytokines including tumor necrotic factor-α and interleukin-1β. In addition, oxidative stress related molecules including superoxide dismutase, catalase, nuclear factor erythroid 2-related factor-2 and heme oxygenase-1 were also increased by hesperidin treatment. Furthermore, Fe 2+, bilirubin and p38 mitogen activated protein kinase, these by-product of heme catabolism in serum and spinal cord of rats with hesperidin-treatment groups were significantly increased compared with those of vehicle-treatment group. Collectively, this study implies that hesperidin accelerates recovery of locomotor function and tissue repair of damaged spinal cord, with concurrent upregulation of heme oxygenase-1 as far as rat SCI model is concerned.