Protective Effect and Mechanism of Total Flavones from Rhododendron simsii Planch on Endothelium-Dependent Dilatation and Hyperpolarization in Cerebral Ischemia-Reperfusion and Correlation to Hydrogen Sulphide Release in Rats

Figure 1

The dilatation (a) and hyperpolarization (b) of middle cerebral arteries of rats subjected to cerebral ischemia-reperfusion to TFR in the presence of 30 μM L-NAME (an inhibitor of nitric oxide synthase) and 10 μM Indo (an inhibitor of cyclooxygenase); effect of TEA (1 mM, an inhibitor of Ca²⁺-activated potassium channel) or PPG (100 μM, an inhibitor of cystathionine-γ-lyase) on non-NO and non-PGI₂-mediated vasodilation (c) and hyperpolarization (d) elicited by TFR in VSMC from middle cerebral artery of rats subjected to cerebral ischemia-reperfusion; effect of endothelial denudation on the dilatation (e) and hyperpolarization (f) to TFR in middle cerebral arteries of rats subjected to cerebral ischemia reperfusion. Values are presented as means ± SE. +Endo: endothelium-intact and −Endo: endothelium-denudated. ^∗∗𝑃<0.01 compared with vehicle group; ^##𝑃<0.01 compared with L-NAME+Indo group; ^▲▲𝑃<0.01 compared with TFR (+Endo) group. Comparisons were performed by unpaired Student’s 𝑡-test.

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