Abstract
The aim of this study was to explore the effect of picroside II on neuronal apoptosis and the expression of caspase-3 and poly ADP-ribose polymerase (PARP) following middle cerebral artery occlusion/reperfusion in male Wistar rats. Picroside II (10 mg/kg) was administered intravenously into the tail vein of the animals. The neurological function deficits were evaluated with the Bederson’s test and the cerebral infarction volume was visualized with tetrazolium chloride (TTC) staining. The apoptotic cells were counted by in situ terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL) assay. The immunohistochemistry stain and enzyme linked immunosorbent assay (ELISA) was used to determine the expressions of caspase-3 and PARP in brain tissue. The results indicated that rats in the control group showed neurological function deficit and cerebral infarction in ischemic hemisphere after two hours ischemia followed by 22 hours reperfusion. Caspase-3 and PARP expressions were also profound in the cortex, the striatum and the hippocampus, along with increased apoptotic cells in this group. Bederson’s score, infarction volume, and expressions of caspase-3 and PARP, as well as apoptosis in the treatment group were, however, significantly decreased compared to those in the control group indicating that intravenous treatment with picroside II might be beneficial to inhibit neuronal apoptosis and, thus, to improve the neurological function of rats upon cerebral ischemia reperfusion injury.
Highlights
Studies have shown that the caspase-family is the promoter and implementer of apoptosis in mammalian cells, among which, caspase-3 is the most critical downstream apoptosis protease in the caspase cascade "waterfall" [1]
The present study aims to explore the properties of picroside II in rat model of focal cerebral ischemia
A major isoflavonoid derived from the Chinese medical herb kudzu root can significantly reduce apoptosis and inhibit caspase-3 activity in dorsolateral cortex in the rat brain of 2 h cerebral ischemia followed by 46 h reperfusion [21]
Summary
Studies have shown that the caspase-family is the promoter and implementer of apoptosis in mammalian cells, among which, caspase-3 is the most critical downstream apoptosis protease in the caspase cascade "waterfall" [1]. Activation of caspase-8 and caspase-9 promote caspase-3, which in turn hydrolyzes cell-specific proteins, and poly ADP ribose polymerase (PARP), thereby inducing apoptosis [2,3]. The plant Picrorhiza scrophulariiflora (Scrophulariaceae) grows in a high altitude in certain regions of Tibet and China The roots of this plant are used in traditional Chinese medicine for a number of conditions [4]. Some studies implicate that picroside II protects hepatocytes against injury and counteracts apoptosis through maintaining the integrity of the mitochondria membrane, enhancing the activity of ATPase in mitochondria, thereby modulating the balance of the cell energy metabolism [12,13]. Experiments on animal models indicate that the picroside extract could inhibit apoptosis in ischemic penumbra in rats following middle cerebral artery occlusion and reperfusion (MCAO/R) [17]. The present study aims to explore the properties of picroside II in rat model of focal cerebral ischemia
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