Conclusions
Diversely, H2S exposure reversed these alterations with reduced HDAC activity. Further, PD rats treated with HDAC inhibitor showed a dramatic upsurge in the level of tyrosine hydroxylase, with a decreased level of glial fibrillary acidic protein, α-synuclein, tumor necrosis factor α, and other cytokines. Thus the results of the study suggest that H2S exerts protection via inhibition of HDAC.
Material and methods
To test this notion, 6-hydroxydopamine (6-OHDA) was used to induce PD and sodium hydrogen sulfide (SHS) was used as a H2S donor and tubastatin A (TSA) was tested in an in vivo rat model to delineate the signaling mechanism.
Methods
To test this notion, 6-hydroxydopamine (6-OHDA) was used to induce PD and sodium hydrogen sulfide (SHS) was used as a H2S donor and tubastatin A (TSA) was tested in an in vivo rat model to delineate the signaling mechanism.
Results
Induction of PD in rats demonstrated elevated oxidative stress with an evidenced decrease in antioxidant enzymes, while elevated pro-inflammatory cytokines and inflammatory mediators were observed in the striatum of PD rats compared to controls. On the other hand, elevated (p < 0.01) levels of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), mRNA transcript of HDAC-2, -3, -4, -6 and total histone deacetylase (HDAC) were found with reduced levels of histone acetyltransferase (HAT) in the brain tissues of PD induced rats. Conclusions: Diversely, H2S exposure reversed these alterations with reduced HDAC activity. Further, PD rats treated with HDAC inhibitor showed a dramatic upsurge in the level of tyrosine hydroxylase, with a decreased level of glial fibrillary acidic protein, α-synuclein, tumor necrosis factor α, and other cytokines. Thus the results of the study suggest that H2S exerts protection via inhibition of HDAC.