Protective effect of astaxanthin on acute cerebral infarction in rats

Abstract

The aim of the study was to investigate the effect of astaxanthin and its possible mechanisms on acute cerebral infarction (ACI) in rat model. Male Sprague Dawley rats were randomly divided into sham group, model group, and astaxanthin-treated groups (20, 40, and 80 mg/kg). Neurological examination, the ratio of cerebral edema, and histopathology changes were assessed. Moreover, some oxidative stress markers were obtained for biochemical analysis, and the expression of neurotrophic factors gene was detected by real-time polymerase chain reaction (RT-PCR) method. The results showed that treatment with astaxanthin notably reduced neurological deficit scores and the ratio of cerebral edema compared with the model group. Meanwhile, astaxanthin increased the activity of catalase, superoxide dismutase, and glutathioneperoxidase as well as decreased the content of malondialdehyde in brain tissue. RT-PCR results showed that the expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) mRNA were increased with astaxanthin treatment. The results indicated that astaxanthin could ameliorate ACI followed by suppressing oxidative stress and upregulating the expression of BDNF and NGF mRNA.

Astaxanthin and its Effects in Inflammatory Responses and Inflammation-Associated Diseases: Recent Advances and Future Directions

“…Compared with those in the cerebral ischemia model group (MCAO group), astaxanthin treatment can promote the axonal regeneration and improve the motor function via activating the cAMP/PKA/CREB signaling pathway (Table 1) [55]. For acute cerebral infarction (ACI) rat, the treatment with astaxanthin notably inhibited oxidative stress and increased the mRNA expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), which led to ameliorate ACI (Table 1) [56]. Astaxanthin also protected the brain from oxidative damage and reduced neuronal deficits due to cerebral ischemia reperfusion injury (IRI) ( Table 1) [57].…”

Astaxanthin inhibits homocysteine‑induced endothelial cell dysfunction via the regulation of the reactive oxygen species‑dependent VEGF‑VEGFR2‑FAK signaling pathway

“…These effects were caused by the suppression of oxidative stress and the upregulation of brain-derived neurotrophic factor and nerve growth factor mRNA (22,23). ATX exerted neuroprotective effects against subarachnoid hemorrhage damage that involved the inhibition of MMP-9 expression, the upregulation of Akt/glycogen synthase kinase-3β and the activation of the nuclear factor-like 2-antioxidant responsive element pathway (24–32); however, the protective effects of ATX against Hcy-induced endothelial dysfunction and the underlying mechanism require further investigation.…”

Deneysel Otizm Spektrum Bozukluğu Modeli Oluşturulan Sıçanlarda Likopenin Beyin IL–6, IL–10, FGF–2 ve NGF Düzeyleri Üzerine Etkisi

“…Ayrıca yine bir başka çalışmada NGF düzeylerinin artışının, yeni doğan sıçan yavrularında beynin hipoksik iskemik hasara karşı korunmasında etkili olduğu bildirilmiştir (27). Yine likopen gibi karotenoid ailesinden olan astaksantinin akut serebral infarkt oluşturulan bir sıçan modelinde, katalaz, süperoksit dismutaz ve glutatyon peroksidaz aktivitesini artırdığı ve beyin dokusundaki malondialdehit içeriğini azalttığı, ayrıca beyin kaynaklı nörotrofik faktör (BDNF) ve NGF mRNA ekspresyonunu arttırdığı gösterilmiştir (28).…”