Neuroprotective Effects of Purple Sweet Potato Balinese Cultivar in Wistar Rats With Ischemic Stroke

Abstract

BACKGROUND:Purple sweet potato (Ipomoea Batatas L.) is one of the sources for anthocyanin, which promotes the health through antioxidant, anti-inflammatory, anti-cancer, neuroprotection, and anti-apoptosis activities. Oxidative stress has been shown to be the cause of apoptosis in ischemic stroke.AIM:The objective of this research was to delineate the pleiotropic effects of anthocyanin for neuroprotection during an acute stroke event.METHODS:Anthocyanin was extracted from Balinese cultivar of purple sweet potato and subsequently administered to rat models of induced ischemic stroke (labelled as treatment group), as well as a placebo (labelled as a control group). Several parameters were in turn evaluated, i.e. the activities of anti-apoptotic (Bcl-2) as well as pro-apoptotic (cytochrome c, caspase-3) molecules, and apoptosis rate. Bcl-2 levels were determined using the histochemical method, cytochrome c and caspase-3 via ELISA method, while apoptosis rate was measured by TdT-medicated Dutp-Nick End Labeling (TUNEL) assay.RESULTS:Bcl-2 expression demonstrated significantly higher Bcl-2 expression in the treatment compared with control group (median 31.2 vs. 1.1; p = 0.001). Accordingly, pro-apoptotic cytochrome c and caspase-3 levels were also found significantly lower in the treatment as opposed to control group (mean 4.17 vs. 8.06; p = 0.001; mean 3.81 vs. 8.02; p = 0.001). Ultimately, apoptosis rate was found markedly lower among treatment than control groups (mean 3.81 vs. control 21.97; p = 0.003).CONCLUSION:The results of this study indicated a significant neuroprotective effect of anthocyanin derived from Balinese cultivar of PSP. Anthocyanin was able to increase and reduce anti-apoptotic and pro-apoptotic protein levels, respectively, resulting in lesser cellular apoptotic rate when compared with placebo. The potential mechanism was thought mainly due to its anti-oxidant properties.

Dietary Anthocyanins and Stroke: A Review of Pharmacokinetic and Pharmacodynamic Studies

“…Both models of ischemia induction (global and focal) were applied in studies on the effects of ACN administration. Some studies reported their beneficial effect when administered before stroke induction [82,180,181,182,183,184], others after the stroke induction [165,185,186], while a third set of studies monitored the effects of ACN administration before and after stroke induction [81,187,188,189].…”

“…In experimental models the brain infarct volume and the apoptotic neurons provoked by induced stroke followed by reperfusion could be reduced by previous administration of ACNs [183]. Studies regarding the effect of pre-administration of ACNs on stroke used purified ACNs [82,181,182] or even encapsulated ACNs available on the market [183] (Table 4) with the aim to elucidate the molecular mechanisms by which ACNs act (see Section 4). Two modalities of stroke induction were applied, most often used is MCA occlusion model of focal ischemia [82,180,181,182,183] and only a single study used bilateral common carotid artery occlusion (BCCAO), which is a model of global ischemia [184], while various ways to administer ACNs are applied (Table 4).…”

“…Studies regarding the effect of pre-administration of ACNs on stroke used purified ACNs [82,181,182] or even encapsulated ACNs available on the market [183] (Table 4) with the aim to elucidate the molecular mechanisms by which ACNs act (see Section 4). Two modalities of stroke induction were applied, most often used is MCA occlusion model of focal ischemia [82,180,181,182,183] and only a single study used bilateral common carotid artery occlusion (BCCAO), which is a model of global ischemia [184], while various ways to administer ACNs are applied (Table 4). In most experimental models, laboratory animals were tracked and subsequently sacrificed 24 h after reperfusion [82,182,183] and only in one study after 72 h [184].…”

“…A comparison between 24 h and 72 h after reperfusion was only revealed by Dewi [180]. Rats were the most used laboratory animals in these studies [82,181,183,184] and less often mice [182]. On the other hand, there is a wide variety in the parameters monitored in these latter studies (neurological, biochemical, histopathological, etc.).…”

“…It was determined that ACNs also inhibit apoptosis rate, measured by TUNEL assay (TdT-medicated dUTP-Nick End Labeling assay) [181,183] and two studies reported that ACNs could have anti-apoptotic activities, as shown by the increase of Bcl-2 (B-cell lymphoma) expression protein, which is known for the involvement in apoptosis regulation [82,181]. A reduction of apoptosis has been recently reported in cerebellum [180] by an immunohistochemistry approach, using an in situ apoptotic detection method.…”