A Review on Neuroinflammatory Pathway Mediating Through Ang-II/AT1 Receptors and a Novel Approach for the Treatment of Cerebral Ischemia in Combination with ARB's and Ceftriaxone.
Gaddam Narasimha RaoSrikanth JupudiJustin AntonyPublished in: Annals of neurosciences (2023)
During cerebral ischemia, an impairment or dysfunction of EAAT-2 attributes the risk of delayed neuronal cell death. Earlier studies evidencing that angiotensin receptor blockers (ARB) attenuate neuroinflammation by inhibiting the Ang-II/AT1 receptor-mediated inflammatory pathway and that ceftriaxone ameliorates the excitotoxicity-induced neuronal deterioration by enhancing the transcription and expression of EAAT-2 via the nuclear transcriptional factor kappa-B (NF-kB) signaling pathway. The present review will briefly discuss the mechanisms involved in Ang-II/AT1-mediated neuroinflammation, ceftriaxone-induced EAAT-2 expression, and the repurposing hypothesis of the novel combination of ARBs and ceftriaxone for the treatment of cerebral ischemia.
Keyphrases
- cerebral ischemia
- subarachnoid hemorrhage
- blood brain barrier
- signaling pathway
- brain injury
- angiotensin ii
- cell death
- poor prognosis
- oxidative stress
- high glucose
- diabetic rats
- angiotensin converting enzyme
- pi k akt
- nuclear factor
- transcription factor
- traumatic brain injury
- long non coding rna
- toll like receptor
- endothelial cells
- inflammatory response
- cell proliferation