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

Increased plasma levels of homocysteine (Hcy) can cause severe damage to vascular endothelial cells. Hcy‑induced endothelial cell dysfunction contributes to the occurrence and development of human cerebrovascular diseases (CVDs). Our previous studies have revealed that astaxanthin (ATX) exhibits novel cardioprotective activity against Hcy‑induced cardiotoxicity in vitro and in vivo.

Clinical efficacy of collateral circulation in the evaluation of endovascular treatment for acute internal carotid artery occlusion.

Objectives: Despite successful recanalization, there remain many patients suffering bad outcome after endovascular treatment, especially for occlusion at the distal portion of internal carotid artery. The goal of the current study was to investigate the value of collateral circulation in predicting malignant events after endovascular treatment in acute ischemic stroke-terminal internal carotid artery (AIS-TICA) patients.

Methods: The records of forty-one patients with AIS-TICA as confirmed by digital subtraction angiography and subjected to mechanical thrombectomy were reviewed.

Correction to: Reversal of homocysteine-induced neurotoxicity in rat hippocampal neurons by astaxanthin: evidences for mitochondrial dysfunction and signaling crosstalk.

[This corrects the article DOI: 10.1038/s41420-018-0114-x.].

Reversal of homocysteine-induced neurotoxicity in rat hippocampal neurons by astaxanthin: evidences for mitochondrial dysfunction and signaling crosstalk.

Elevated plasma level of homocysteine (Hcy) represents an independent risk for neurological diseases, and induction of oxidative damage is considered as one of the most important pathomechanisms. Astaxanthin (ATX) exhibits strong antioxidant activity in kinds of experimental models. However, the potential of ATX against Hcy-induced neurotoxicity has not been well explored yet.

Selenocysteine antagonizes oxygen glucose deprivation-induced damage to hippocampal neurons.

Designing and/or searching for novel antioxidants against oxygen glucose deprivation (OGD)-induced oxidative damage represents an effective strategy for the treatment of human ischemic stroke. Selenium is an essential trace element, which is beneficial in the chemoprevention and chemotherapy of cerebral ischemic stroke. The underlying mechanisms for its therapeutic effects, however, are not well documented.