Levistolide A

Levistolide A is an apoptosis inducer and a PEDV virus inhibitor. Levistolide A can induce apoptosis in colon cancer cells and suppress the replication of porcine epidemic diarrhea virus (PEDV) by promoting ROS generation. Levistolide A activates peroxisome proliferator-activated receptor γ (PPARγ) in N2a/APP695swe cells and reduces excessive phosphorylation of tau through the GSK3α/β pathway, improving symptoms in Alzheimer’s mice. Levistolide A improves kidney damage in 5/6 nephrectomy (Nx) mice by inhibiting the RAS,TGF-β1/Smad, and MAPK pathways^[1][2][3][4].
In Vitro:Levistolide A (50, 100 μM; 24 h) induces apoptosis in colon cancer cells by promoting ROS generation and mediating the endoplasmic reticulum stress pathway^[1].
Levistolide A (1.1, 3.3, 10 μg/mL) activates peroxisome proliferator activated receptor gamma (PPARγ) in N2a/APP695swe cells and reduces tau hyperphosphorylation through the GSK3 α/β pathway, thereby reducing the production and aggregation of β - amyloid protein (A β)^[2].
Levistolide A (20-80 μM; 36 h) can inhibit the replication of Porcine Epidemic Diarrhea Virus (PEDV) by inducing ROS generation^[3].
In Vivo:Levistolide A (2 mg/kg; once every two days; i.p.) can improve memory deficits and cognitive abilities in Alzheimer's disease mice, and reduce inflammatory responses in the brain^[2].
Levistolide A (0.5-2 mg/kg; once every two days; 4 weeks; i.p.) improves renal fibrosis and injury in 5/6 nephrectomy (Nx) mice by inhibiting the expression of key molecules in the RAS, TGF - β 1/Smad, and MAPK pathways^[4].