Antidiabetic Drugs Can Reduce the Harmful Impact of Chronic Smoking on Post-Traumatic Brain Injuries.
Farzane SivandzadeFaleh AlqahtaniHemangini A DhaibarDiana Cruz-TopeteLuca CuculloPublished in: International journal of molecular sciences (2023)
Traumatic Brain Injury (TBI) is a primary cause of cerebrovascular and neurological disorders worldwide. The current scientific researchers believe that premorbid conditions such as tobacco smoking (TS) can exacerbate post-TBI brain injury and negatively affect recovery. This is related to vascular endothelial dysfunction resulting from the exposure to TS-released reactive oxygen species (ROS), nicotine, and oxidative stress (OS) stimuli impacting the blood-brain barrier (BBB) endothelium. Interestingly, these pathogenic modulators of BBB impairment are similar to those associated with hyperglycemia. Antidiabetic drugs such as metformin (MF) and rosiglitazone (RSG) were shown to prevent/reduce BBB damage promoted by chronic TS exposure. Thus, using in vivo approaches, we evaluated the effectiveness of post-TBI treatment with MF or RSG to reduce the TS-enhancement of BBB damage and brain injury after TBI. For this purpose, we employed an in vivo weight-drop TBI model using male C57BL/6J mice chronically exposed to TS with and without post-traumatic treatment with MF or RSG. Our results revealed that these antidiabetic drugs counteracted TS-promoted downregulation of nuclear factor erythroid 2-related factor 2 (NRF2) expression and concomitantly dampened TS-enhanced OS, inflammation, and loss of BBB integrity following TBI. In conclusion, our findings suggest that MF and RSG could reduce the harmful impact of chronic smoking on post-traumatic brain injuries.
Keyphrases
- traumatic brain injury
- brain injury
- oxidative stress
- blood brain barrier
- cerebral ischemia
- subarachnoid hemorrhage
- severe traumatic brain injury
- reactive oxygen species
- smoking cessation
- nuclear factor
- mild traumatic brain injury
- drug induced
- diabetic rats
- systematic review
- nitric oxide
- toll like receptor
- body mass index
- cell proliferation
- resting state
- ischemia reperfusion injury
- white matter
- physical activity
- type diabetes
- cell death
- induced apoptosis
- body weight
- adipose tissue
- functional connectivity
- immune response
- long non coding rna
- metabolic syndrome
- heat shock protein