The Antinociceptive Effects of Combined Treatment With Atorvastatin and Vitamin C in the Chronic Constriction Injury Model of Rats.
Abolfazl AbbaszadehNajmeh PirzadroozbahaniMahmood Reza MoradkhaniAmin HasanvandPublished in: Basic and clinical neuroscience (2023)
Nerve damage causes the deposition of inflammatory factors and or oxidative stress at the site of injury, which in turn activates glial cells that are involved in increasing the inflammatory process by producing and releasing pro-inflammatory agents and oxidative stress. Among statins, atorvastatin is a drug to reduce inflammation, and its effectiveness has been recorded as an antioxidant effect. Vitamin C is known as a neuroprotective agent. Ascorbate inhibits the production of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in monocytes in high doses (20 mM) by inhibiting them. The rats were randomly divided into 7 groups of 10 animals as follows: 1: Sham-operated, 2: Chronic constriction injury (CCI), 3: CCI+vitamin C (500 mg/kg), 4: CCI+atorvastatin (5 mg/kg), 5: CCI+atorvastatin (10 mg/kg), 6: CCI+vitamin C (500 mg/kg)+atorvastatin (5 mg/kg), and 7: CCI+vitamin C (500 mg/kg)+atorvastatin (10 mg/kg). The results of the present study indicated that the anti-inflammatory, antioxidant, and neuroprotective properties of vitamin C and atorvastatin improved the effects of CCI in an empirical neuropathic in rats. Moreover, it was shown that the associated treatment with vitamin C and atorvastatin can reduce inflammatory factors, such as TNF-α and IL-6, and oxidative markers, such as glutathione peroxidase (GPx), superoxide dismutase (SOD), and malonaldehyde (MDA), while the nerve conduction velocity enhanced and inflammation decreased in histology studies in CCI rats.
Keyphrases
- neuropathic pain
- oxidative stress
- spinal cord
- spinal cord injury
- induced apoptosis
- anti inflammatory
- diabetic rats
- ischemia reperfusion injury
- dna damage
- rheumatoid arthritis
- randomized controlled trial
- systematic review
- cardiovascular disease
- cerebral ischemia
- clinical trial
- cell cycle arrest
- cell proliferation
- hydrogen peroxide
- drug induced
- subarachnoid hemorrhage
- dendritic cells
- blood brain barrier
- cell death
- blood flow
- double blind
- quantum dots
- brain injury
- peripheral nerve