The polysaccharide-protein complexes found in PL have immunomodulating (1), anti-angiogenic, and antioxidant and xanthine oxidase inhibition effects (5). Additionally, the furopyranone compounds inhibit protein glycation, which may aid in treatment and prevention of diabetic complications (4) (23). In non-obese diabetic mice, a polysaccharide extract from PL enhanced function of macrophages, dendritic cells, NK cells, T cells and B cells, prevented inflammation by inhibiting IFN-gamma, IL-2 and TNF-alpha by TH1 cells and macrophages; it also upregulated IL-4 expression in TH2 cells. These effects may help prevent diabetes (23). The anti-inflammatory activities of inotilone, a compound isolated from PL might be due to reduced levels of malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), COX-2, NF-κB, and matrix metalloproteinase (MMP)-9, and via increased activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) through the suppression of TNF-α and nitric oxide (NO) (25).
In another study, hispidin, a phenolic compound present in PL, was shown to protect against peroxynitrite-mediated cytotoxicity, DNA damage and hydroxyl radical formation (26).
PL also inhibited proliferation of SW480, a human colon cancer cell line via decreasing Bcl-2 and cyclin B1, and increasing cytochrome C (9). Another study similarly found that a PL extract induced G0/G1 arrest and apoptosis in human colon carcinoma HT29 cells, through p21(C1P1/WAF1) upregulation, cyclin D1 downregulation, Bcl2 downregulation, release of cytochrome C and activation of caspases 9, 3 and 8 (10). Decrease in cyclin-dependent kinases CDK2, 4 and 6, and dose-dependent apoptosis of lung cancer cells after treatment with PL were also observed (12). Further, it suppressed aryl hydrocarbon receptor activity and AhR-dependent gene expression, both pathways activated by cigarette smoking (13).