Pinusolide

Pinusolide is an AMPK activator and PAF receptor antagonist. Pinusolide activates AMPK, phosphorylates ACC, enhances IRS-1 tyrosine phosphorylation, boosts glucose uptake, and modulates insulin signaling. Pinusolide inhibits caspase-3/7 activation, intracellular calcium elevation, reactive oxygen species overproduction, lipid peroxidation, and tumor cell proliferation. Pinusolide stabilizes superoxide dismutase activity, reduces apoptotic hallmarks, induces mitochondrial pathway apoptosis, and triggers DNA fragmentation. Pinusolide can be used for the research of type 2 diabetes, neurodegenerative diseases, acute lymphoblastic leukemia, acute myeloid leukemia, and Burkitt lymphoma^[1][2][3]. In Vitro:Pinusolide (10-100 μM; 24 h) is non-cytotoxic to L6 myotubes at concentrations up to 100 μM^[1].
Pinusolide (10-20 μM; 0.5-24 h) dose-dependently and time-dependently increases AMPK and ACC phosphorylation in L6 myotubes, with peak effects at 20 μM for 2 h and 10 μM at 2 h respectively^[1].
Pinusolide (10-20 μM; 2 h) significantly increases glucose uptake in L6 myotubes, with 72% and 78% induction at 10 μM and 20 μM respectively after 2 h incubation^[1].
Pinusolide (10 μM; 2 h) has its induced AMPK/ACC phosphorylation blocked and mediated glucose uptake reduced by Compound C (HY-13418A) in L6 myotubes, confirming AMPK dependence^[1].
Pinusolide (10 μM; 2 h) requires LKB1 for induced AMPK activation and glucose uptake in L6 myotubes^[1].
Pinusolide (10 μM; 2 h) improves high glucose-induced insulin resistance in L6 myotubes by restoring AMPK activation, reducing JNK phosphorylation, and reinstating insulin-stimulated IRS-1/Akt phosphorylation and glucose uptake^[1].
Pinusolide (10 μM; 2 h) improves high glucose-induced insulin resistance in L6 myotubes via an AMPK-dependent mechanism, as AMPKα2 knockdown abolishes all beneficial effects^[1].
Pinusolide (5.0 μM; 1 h pretreatment, 18 h STS exposure) protects primary mixed rat cortical cells from staurosporine-induced apoptotic morphological changes^[2].
Pinusolide (1.0-5.0 μM; 1 h pretreatment, 18 h STS exposure) preserves superoxide dismutase activity reduced by staurosporine in primary rat cortical cells, with greater preservation at 5.0 μM^[2].
Pinusolide (1.0-5.0 μM; 1 h pretreatment, 12 h STS exposure) reduces staurosporine-induced caspase-3/7 activation in primary rat cortical cells^[2].
Pinusolide (5-100 μM; 24-48 h) inhibits the proliferation of Burkitt lymphoma BJAB cells in a concentration-dependent manner, with up to 44% inhibition after 24 h and up to 86% inhibition after 48 h of treatment^[3].
Pinusolide (50-100 μM; 48 h) induces mitochondrial permeability transition in Burkitt lymphoma BJAB cells, with 86.36% of cells exhibiting low mitochondrial membrane potential after 48 h treatment with 100 μM pinusolide^[3].
Pinusolide (50-100 μM; 72 h) induces apoptosis in Burkitt lymphoma BJAB cells, with 69.52% of cells showing DNA fragmentation after 72 h treatment with 100 μM pinusolide, accompanied by characteristic apoptotic morphological changes^[3].