Paederosidic acid has significant anti-tumor, anticonvulsant and sedative effects. Paederosidic acid increases brain gamma-aminobutyric acid and decreases glutamic acid in the brain, and it up-regulates expressions of GAD 65, may be a promising future therapeutic agent for treatment of epilepsy.

Paederosidic acid（PA）在体外对肺癌显示出显著的抗肿瘤活性；其机制涉及通过上调caspase-3、caspase-8、caspase-9、Bid、Bax的表达，下调Bcl-2的表达以及促进Cyto-C从线粒体释放，进而诱导线粒体介导的凋亡。在A549细胞中，PA处理后JNK磷酸化水平显著增加，而Akt磷酸化水平相应减少。然而，JNK siRNA转染的细胞减弱了PA诱导的caspase-3、8、9、Bid以及Bax的激活，同时增强了Bcl-2的激活。PA诱导的JNK激活在凋亡中发挥了重要的功能作用。

从Paederia scandens (Lour.) Merrill中分离出的paederosidic acid在小鼠和大鼠中展现了显著的抗惊厥和镇静效果。通过以5, 10, 20, 以及40 mg/kg的剂量（ip注射）给药，发现paederosidic acid能显著提高大脑中的γ-氨基丁酸水平并降低谷氨酸水平，同时上调GAD 65的表达。因此，paederosidic acid可能是治疗癫痫的有前景的未来治疗剂[2]。

The anti-proliferative effects of PA on A549 cells were evaluated by MTT method and the IC50 values were calculated. Furthermore, the PA-induced apoptosis in A549 cells was determined by fluorescence microscope via staining with DAPI and by flow cytometer via staining with FITC conjugated Annexin V/PI. The expression of apoptosis-related or signaling proteins was investigated by Western blotting[1]

Anticonvulsant activities of paederosidic acid were evaluated by maximal electroshock and pentylenetetrazole-induced seizures in male mice. Then, pentobarbital sodium-induced sleeping time and locomotor activity tests in mice were used to evaluate the sedative effects of paederosidic acid. Finally, the mechanism of paederosidic acid was explored by evaluating the contents of Glu and GABA in the brain, and Western blot was used to measure GAD65 expression in the mouse brain[2].