In comparison to MCAO group, DAHP suppressed the expressions of apoptotic cytokines, caspase-3, TNF-[alpha], and iNOS (* P < 0.05 versus DAHP-treated group); however, expressions of antiapoptotic cytokines, Bcl-2, and COX-2 were stimulated (*P <0.05 versus the DAHP-treated group) (Figure 5).
In comparison to MCAO group, expressions of apoptotic cytokines, caspase-3, TNF-[alpha], and iNOS were suppressed by DAHP (* P < 0.05 and ** P <0.05 versus DAHP-treated group) (Figures 6(a), 6(c), and 6(d)).
We evidence neuroprotectiveness of DAHP in an MCAO rat model and report our findings following Western blot and immunohistochemical analyses as well as TUNEL staining.
In this study, iNOS expression was suppressed via DAHP which is possibly due to inhibition of GTPCH 1 activity to decrease BH4 synthesis.
In essence, apoptosis plays an essential role in stroke pathology, while DAHP treatment markedly decreased caspase-3 protein in our study; thus, DAHP neuroprotective effects might arise following suppression of proapoptotic factors.
In our study, COX-2 expression was upregulated more in DAHP group than in MCAO and DMSO groups.
In summation, DAHP attenuates brain injury in a rat model through iNOS signaling pathway as well as apoptosis.
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Fang, "Neuroprotective effects of DAHP and triptolide in focal cerebral ischemia via apoptosis inhibition and PI3K/Akt/mTOR pathway activation," Frontiers in Neuroanatomy, vol.
DAHP downregulated the expression levels of caspase-3, TNF-[alpha], and iNOS, but upregulated the levels of Bcl-2 and COX-2, when compared with the MCAO group.