{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T11:25:11Z","timestamp":1788261911146,"version":"build-2803163510"},"reference-count":31,"publisher":"World Scientific Pub Co Pte Ltd","issue":"03","funder":[{"name":"Health and Family Planning Commission of Hebei","award":["20190123"],"award-info":[{"award-number":["20190123"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Am. J. Chin. Med."],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:p>Stroke has become a major cause of death and disability worldwide. The cellular recycling pathway autophagy has been implicated in ischemia-induced neuronal changes, but whether autophagy plays a beneficial or detrimental role is controversial. Hydroxysafflor Yellow A (HSYA), a popular herbal medicine, is an extract of Carthamus tinctorius and is used to treat ischemic stroke (IS) in China. HSYA has been shown to prevent cardiovascular and cerebral ischemia\/reperfusion injury in animal models. However, the specific active ingredients and molecular mechanisms of HSYA in IS remain unclear. Here, we investigated the effect of HSYA treatment on autophagy in a rat model of IS. IS was induced in rats by middle cerebral artery occlusion. Rats were treated once daily for 3 days with saline, HYSA, or the neuroprotective agent Edaravone. Neurobehavioral testing was performed on days 1, 2, and 3 post-surgery. Brains were removed on day 3 post-surgery for histological evaluation of infarct area, morphology, and for qRT-PCR and western blot analysis of the expression of the autophagy factor LC3 and the signaling molecules HIF-1[Formula: see text], BNIP3, and Notch1. Molecular docking studies were performed in silico to predict potential interactions between HSYA and LC3, HIF-1[Formula: see text], BNIP3, and Notch1 proteins. The result showed that HSYA treatment markedly alleviated IS-induced neurobehavioral deficits and reduced brain infarct area and tissue damage. HSYA also significantly reduced hippocampal expression levels of LC3, HIF-1[Formula: see text], BNIP3, and Notch1. The beneficial effect of HSYA was generally superior to that of Edaravone. Molecular modeling suggested that HSYA may bind strongly to HIF-1[Formula: see text], BNIP3, and Notch1 but weakly to LC3. In conclusion, HSYA inhibits post-IS autophagy induction in the brain, possibly by suppressing HIF-1[Formula: see text], BNIP3 and Notch1. HSYA may have utility as a post-IS neuroprotective agent.<\/jats:p>","DOI":"10.1142\/s0192415x22500331","type":"journal-article","created":{"date-parts":[[2022,3,18]],"date-time":"2022-03-18T05:41:24Z","timestamp":1647582084000},"page":"799-815","source":"Crossref","is-referenced-by-count":24,"title":["Hydroxysafflor Yellow A Alleviates Ischemic Stroke in Rats via HIF-1\u03b1, BNIP3, and Notch1-Mediated Inhibition of Autophagy"],"prefix":"10.1142","volume":"50","author":[{"given":"Yuliang","family":"Zhang","sequence":"first","affiliation":[{"name":"College of Traditional Chinese Medicine, Hebei University, Baoding, Hebei 071000, P. R. China"},{"name":"Langfang TCM Hospital, Langfang, Hebei 065000, P. R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Liu","sequence":"additional","affiliation":[{"name":"College of Traditional Chinese Medicine, Hebei University, Baoding, Hebei 071000, P. R. 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