Tavarua Deoxyriboside A and Jasplakinolide as Potential Neuroprotective Agents: Effects on Cellular Models of Oxidative Stress and Neuroinflammation.
Rebeca AlvariñoEva AlonsoJioji N TabudravuNadia Pérez-FuentesAmparo AlfonsoLuis M BotanaPublished in: ACS chemical neuroscience (2020)
The oceans harbor a great reservoir of molecules with unknown bioactivities, which could be useful for the treatment of illnesses that nowadays have no cure, such as neurodegenerative diseases. In this work, we evaluated the neuroprotective potential of the marine Fijian compounds tavarua deoxyriboside A and jasplakinolide against oxidative stress and neuroinflammation, crucial mechanisms in neurodegeneration. Both metabolites protected SH-SY5Y human neuroblastoma cells from H2O2 damage, improving mitochondrial function and activating the antioxidant systems of cells. These effects were mediated by their ability of inducing Nrf2 translocation. In BV2 microglial cells activated with lipopolysaccharide, Fijian metabolites also displayed promising results, decreasing the release of proinflammatory mediators (ROS, NO, cytokines) through the reduction of gp91 and NFkB-p65 expression. Finally, we performed a coculture among both cell lines, in which treatment with compounds protected SH-SY5Y cells from activated microglia, corroborating their neuroprotective effects. These results suggest that tavarua deoxyriboside A and jasplakinolide could be used as candidate molecules for further studies against neurodegeneration.
Keyphrases
- oxidative stress
- induced apoptosis
- lps induced
- lipopolysaccharide induced
- inflammatory response
- dna damage
- cerebral ischemia
- cell cycle arrest
- signaling pathway
- ischemia reperfusion injury
- traumatic brain injury
- endothelial cells
- ms ms
- cell death
- poor prognosis
- diabetic rats
- neuropathic pain
- toll like receptor
- immune response
- combination therapy
- anti inflammatory
- climate change
- long non coding rna
- pluripotent stem cells
- cell proliferation