Andrographolide (AP) is a NF-κB inhibitor, which inhibits NF-κB activation through covalent modification of a cysteine residue on p50 in endothelial cells without affecting IκBα degradation or p50/p65 nuclear translocation. Treatment with Andrographolide (5 or 30mg/kg) reduces the extent of bone loss induced by LPS. Moreover, Andrographolide slightly increases the BMD and cortex thickness compared to LPS treatment[3]. Andrographolide ameliorates RILI by suppressing AIM2 inflammasome mediated-pyroptosis in macrophage, identifying Andrographolide as a novel potential protective agent for RILI(Radiation-induced lung injury)[4]. Andrographolide administration improved behavioural deficits and attenuated loss of dopaminergic neurons in MPTP-exposed mice and reduced cell death induced by rotenone in vitro. Andrographolide bound to DRP1 and inhibited its GTPase activity, thereby preventing excessive mitochondria fission and neuronal damage in PD[5]. Andr (Andrographolide) markedly attenuated cardiac fibrosis and relieved inflammation after myocardial infarction. Andr significantly blocked oxidative stress and the nuclear translocation of p-P65 following myocardial infarction[6].
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