Polyphenols Targeting Oxidative Stress in Spinal Cord Injury: Current Status and Future Vision

Abstract

A spinal cord injury (SCI) occurs when the spinal cord is deteriorated or traumatized, leading to motor and sensory functions lost even totally or partially. An imbalance within the generation of reactive oxygen species and antioxidant defense levels results in oxidative stress (OS) and neuroinflammation. After SCI, OS and occurring pathways of inflammations are significant strenuous drivers of cross-linked dysregulated pathways. It emphasizes the significance of multitarget therapy in combating SCI consequences. Polyphenols, which are secondary metabolites originating from plants, have the promise to be used as alternative therapeutic agents to treat SCI. Secondary metabolites have activity on neuroinflammatory, neuronal OS, and extrinsic axonal dysregulated pathways during the early stages of SCI. Experimental and clinical investigations have noted the possible importance of phenolic compounds as important phytochemicals in moderating upstream dysregulated OS/inflammatory signaling mediators and axonal regeneration’s extrinsic pathways after the SCI probable significance of phenolic compounds as important phytochemicals in mediating upstream dysregulated OS/inflammatory signaling mediators. Furthermore, combining polyphenols could be a way to lessen the effects of SCI.

Encapsulation of Selenium Nanoparticles and Metformin in Macrophage-Derived Cell Membranes for the Treatment of Spinal Cord Injury

“…Recent studies have shown that oxidative stress is involved in a series of neurological diseases, including cerebral ischemia, SCI, and Alzheimer’s disease. − Many studies have confirmed that excessive ROS can exacerbate SCI . Excessive ROS production can cause severe damage to proteins and DNA in spinal cord tissue, ultimately leading to increased inflammation and neuronal cell death. , ROS, GSH, SOD, and MDA are widely used as markers of oxidative stress after SCI. , In the present study, both in vitro and in vivo experiments showed that SeNPs-Met-MVs could be a key regulator of neuroprotection in response to oxidative stress. It was confirmed by immunofluorescence experiments that SeNPs-Met-MVs could reduce the expression of the HIF-1α, regulate the hypoxic environment, and are a key regulator of neuroprotection in response to oxidative stress.…”

“…46 Excessive ROS production can cause severe damage to proteins and DNA in spinal cord tissue, ultimately leading to increased inflammation and neuronal cell death. 47,48 ROS, GSH, SOD, and MDA are widely used as markers of oxidative stress after SCI. 49,50 In the present study, both in vitro and in vivo experiments showed that SeNPs-Met-MVs could be a key regulator of neuroprotection in response to oxidative stress.…”

Natural product-based pharmacological studies for neurological disorders

“…High-performance liquid chromatography in conjunction with photodiode array detection, electrospray ionization-mass spectrometry, and phytochemical fingerprinting of JSK was used. Additionally, JSK seems to target several pathways (biochemical and cellular) to promote functional recovery and enhance the results of SCI ( Su et al, 2013 ; Islam et al, 2022 ). To evaluate the therapeutic effects of ethanolic extract of Mucuna pruriens (MP) in treating SCI, Chandran et al used the widely researched standardized Multicenter Animal Spinal Cord Injury Study animal model of the contusive spinal cord.…”

ACOD1, rather than itaconate, facilitates p62‐mediated activation of Nrf2 in microglia post spinal cord contusion

“…Traumatic spinal cord injury (SCI) causes acute mechanical contusion of neural tissue and induces prominent neuroinflammation, a characteristic that is evident in brain injury and other acute neurological diseases 1,2 . Neuroinflammation and oxidative stress (OS) following SCI trigger secondary neuropathies such as glial accumulation, neuronal loss, and demyelination that exacerbate neurological dysfunction and functional disorder 3–5 . Microglia are the resident immune cell of the central nervous system and become activated immediately after a trauma, and have been recognised as one of the key mediators of neuroinflammation in the acute phase of SCI 6,7 .…”

“… 1 , 2 Neuroinflammation and oxidative stress (OS) following SCI trigger secondary neuropathies such as glial accumulation, neuronal loss, and demyelination that exacerbate neurological dysfunction and functional disorder. 3 , 4 , 5 Microglia are the resident immune cell of the central nervous system and become activated immediately after a trauma, and have been recognised as one of the key mediators of neuroinflammation in the acute phase of SCI. 6 , 7 Moreover, microglia actively produce multiple oxidisers including nitric oxide (NO) and reactive oxygen species (ROS) that contribute to neurotoxicity.…”