TL;DR
It is suggested that Gomisin A exerts neuroprotective effects against CIRI by enhancing angiogenic activity while attenuating oxidative stress and apoptosis, partly through activation of the VEGF/PI3K/AKT/NOS3 pathway.
Findings indicate that TZ may protect against CIRI by suppressing apoptosis and neuroinflammation through activation of the PI3K/AKT/mTOR signaling pathway, thereby providing preclinical evidence for its potential repurposing as a treatment for ischemic stroke.
Findings indicate that Echinocystic acid protects against CIRI, at least in part, through a PPARγ-dependent mechanism involving promotion of microglial M2 polarization and attenuation of NLRP3/Caspase-1/GSDMD-associated pyroptotic signaling, highlighting the therapeutic potential of EA in CIRI.
It is demonstrated that gastrodin activates AMPK signaling by inhibiting PRMT1 protein expression in BMECs, thereby improving ferroptosis and dysfunction in BMECs and alleviating CIRI.
It is suggested that 4-OI confers Neuroprotection against I/R injury by activating Nrf2 pathway, reducing oxidative stress, and suppressing ferroptotic and apoptotic cell death.
It is demonstrated that kaempferol ameliorates MIRI by activating Nrf2/GPX4-related antioxidant signaling, thereby inhibiting ferroptosis, attenuating apoptosis, reducing myocardial structural damage, and ultimately preserving cardiac function.
IMEG exerts a protective effect against intestinal I/R injury through its antioxidant, anti-inflammatory, and anti-apoptotic properties.
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