1. Nuciferine is a major active aporphine alkaloid from the leaves of N. nucifera Gaertn that possesses anti-hyperlipidemia, anti-hypotensive, anti-arrhythmic, and insulin secretagogue activities.
2. Nuciferine is an important drug candidate for the treatment of obesity-related diseases, through ameliorating HFD-induced dyslipidemia as well as liver steatosis and injury.
3. Nuciferine may be potential for the prevention and treatment of hyperuricemia with kidney inflammation.
4. Nuciferine has a vasorelaxant effect via both endothelium-dependent and -independent mechanisms, suggests that nuciferine may have a therapeutic effect on vascular diseases associated with aberrant vasoconstriction.
5. Nuciferine, extracted from Nelumbo nucifera, can stimulate both phases of insulin secretion in isolated islets by closing potassium-adenosine triphosphate channels, explaining anti-diabetic effects of Nelumbo nucifera.
6. Nuciferine inhibits tumor-promoting effect of nicotine involving Wnt/β-catenin signaling in non-small cell lung cancer, it presents a potential novel alternative to NSCLC prevention and therapy.
1. Pinusolide is a platelet activating factor ( PAF) antagonist, it may prove of therapeutic value in the treatment of hypotension .
2. Pinusolide has antileukemic potential, it not only decreases the proliferation activity of tumor cells at relatively low concentrations but specifically induces apoptosis at 100 microM via the mitochondrial pathway in the Burkitt lymphoma cell line BJAB.
3. Pinusolide attenuates blockade of insulin signaling by enhancing IRS-1 tyrosine phosphorylation by the activating the AMPK pathway, indicates the targeting of AMPK represents a new therapeutic strategy for hyperglycemia-induced insulin resistance and type 2 diabetes.
4. Pinusolide can protect neuronal cells from staurosporine (STS) -induced apoptosis, probably by preventing the increase in [Ca2+]i and cellular oxidation caused by STS, and indicate that it could be used to treat neurodegenerative diseases.
5. Pinusolide shows potent inhibition of 5-LO dependent LTC4 generation, which requires both suppression of calcium influx and JNK phosphorylation.