Berberine modulates AP-1 activity to suppress HPV transcription and downstream signaling to induce growth arrest and apoptosis in cervical cancer cells.
Berberine was also found to inhibit the activity of activator protein 1, a transcription factor that plays a critical role in inflammation and carcinogenesis (Fukuda et al., 1999b).
Berberine, a naturally occurring isoquinoline alkaloid, is present in the roots, rhizome, and stem bark of a number of medicinal plants.
Berberine has tremendous potential to cure many physiological disorders;
hence, it has been used in the Ayurvedic [6], Unani, and Chinese as well as Homeopathic medicine.
Berberine has been shown to inhibit activator protein 1, a key transcription factor in inflammation and carcinogenesis, in human cell lines [7]
and has been shown to possess antitumor properties and effectively inhibit cyclooxygenase-2 transcriptional activity in human colon cancer cells [8, 9].
Berberine is known to inhibit DNA topoisomerase II [10].
Moreover, the antitumor properties of berberine are now recognized by researchers and clinical oncologists.
The effects of berberine on human malignant brain tumor, esophageal cancer, and human leukemic and human colon cancer cell lines have been tested and significant killing effects have been achieved [1, 2, 11].
After looking into all these properties of Berberine, it was decided to try to encapsulate it in NP of PLGA for facilitated drug delivery (Scheme 1).
Many acute and chronic neurodegenerative diseases are characterized by a localized inflammatory response and
constitutive activation of the transcription factors nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) as well as their upstream activating signaling cascades.
These results suggest that by inhibiting NF-κB and AP-1 signaling, compound A is able to reduce tissue inflammation and neuronal cell death, resulting in significant neuroprotection in animal models of neurodegeneration.