reoxygenation

Bisandrographolide C is identified from Andrographis paniculata. Bisandrographolide C activates TRPV1 and TRPV3 channels (Kds: 289 and 341 μM) and protects cardiomyocytes from hypoxia-reoxygenation injury.

CD3254 is a selective and potent retinoid X receptor-like (RXR) agonist that inhibits neuronal cell death with OGD reoxygenation.

HZS60 is a brain-penetrant NMDAR TRPM4 inhibitor that shows promise in ameliorating cerebral ischemia. It provides significant neuroprotection against ischemic injury in primary neurons caused by NMDA and oxygen-glucose deprivation reoxygenation. HZS60 demonstrates favorable pharmacokinetic properties and can inhibit cerebral ischemia-reperfusion injury, positioning it as a potential inhibitor for ischemic stroke.

1400W is a slow, tight-binding, and highly selective inducible nitric-oxide synthase (iNOS) inhibitor, with a K_d value ≤ 7 nM. 1400W inhibits iNOS induction in microglial cells and reduces the generation of NO, thereby mitigating oxidative stress and neuronal cell apoptosis in the rat cerebral cortex, and improving spatial memory dysfunction caused by acute hypobaric hypoxia-reoxygenation [1] [2].

Ferroptosis-IN-10 (compound D1) is an inhibitor of ferroptosis, demonstrating a potent IC50 value of 22 nM. It exhibits neuroprotective activity in the oxygen-glucose deprivation reoxygenation (OGD R) model.

TJ-M2010-5 is a MyD88 inhibitor that binds to the TIR domain to interfere with its homodimerization and suppress MyD88 signaling. TJ-M2010-5 can be used in myocardial [ischemia reperfusion] injury studies.

Ginsenoside Ra1, a component from ginseng, exhibits significant inhibitory effects on protein tyrosine kinase (PTK) activation induced by hypoxia reoxygenation (H R).

Monomethyl lithospermate (Lithospermic acid monomethyl ester) has potential antiviral activity, alleviating ischemic stroke injury in vivo in middle cerebral artery occlusion mice by activating PI5K Akt signaling and protecting oxygen-glucose deprivation reoxygenation-induced SHSY-3Y cells in vitro. Monomethyl lithospermate could improve the viability of SHSY-5Y cells, inhibit mitochondrial membrane potential (MMOP) collapse, and inhibit cell apoptosis. Monomethyl lithospermate also reduced the level of oxidative stress in the brain tissue of middle artery occlusion (MCAO) rats and improved nerve damage in ischemic stroke (IS) rats.