tudies should focus on whether lantadene A suppressed pro-inflammatory transcription factors such as
transcription factor nuclear factor-kB (NF-kB) and NF-IL-6 or activating protein-1 (AP-1). The
transcription factor NFkB regulates the expression of a wide range of genes involved in immune
response, inflammation, and acute phase response, as well as several viral genes. Recent evidence also
suggests that NFkB is involved in carcinogenesis and apoptosis [27]. Moreover, various kinds of
antioxidants have been reported to down-regulate NFkB activation in a wide range of cell types [28]
(Figure 8). Furthermore, lantadene A treatment may up-regulates Bax, down-regulates Bcl-2
expression, promotes Bax translocation to mitochondria, activates mitochondria-mediated apoptotic
pathway, which in turn causes the release of caspase-3, and promote cell apoptosis which deserved
further study (Figure 8). Our previous results on L. camara’s leaf extracts which consist of lantadene A,
did not showed any apparent toxicity towards Vero cells with an IC50 value of 319.37 ± 99.80 µg/mL
at 72 h. However, the results of oral acute toxicity study on L. camara leaf showed a pro-toxic effect.
Hence, further toxicity studies are needed to determine the acute and chronic oral toxicity effects of
lantadene A on animal fetus, pregnant animals, and their reproductive capacity, to complete the safety
profile of this compound which should be very useful for any future in vivo or clinical study of this
compound [29]