The active constituents of andrographis are diterpenoid lactones known as andrographolides ^(10) (11). They exhibit anti-inflammatory activity by inhibiting NO production and COX-2 expression ⁽²⁶⁾. In mouse hepatocytes, andrographis induced mRNA expression of CYP1A1 and 1A2 in a concentration-dependent manner ⁽³¹⁾. In other studies, andrographis extract demonstrated a calcium channel inhibition effect that could cause smooth muscle relaxation, decreased blood pressure and heart rate ⁽³²⁾, and relaxation of the uterus ⁽³³⁾. It also showed antiplatelet effects by inhibiting thrombin ⁽³⁴⁾ and platelet activating factor ⁽³⁵⁾. When given orally to mice, andrographis extract neutralized snake venom ⁽⁹⁾.

In other preclinical studies, activity against multiple myeloma cells may occur via TLR4/NF-kappaB signaling pathway inhibition ⁽⁵²⁾. In human colorectal cancer cells, reversal of 5-FU resistance was attributed to elevated BAX expression ⁽⁵⁰⁾. Migration and invasion was inhibited through suppression of mRNA and MMP-7 protein levels ⁽¹³⁾, while MMP-2 activity was also identified ⁽¹⁴⁾. Inhibition of IL-6 expression and IL-6-mediated signals occurred in human prostate cancer cells ⁽¹²⁾. In non-small cell lung cancer cells andrographolides reduced invasiveness by suppressing the PI3K/Akt/AP-1 signaling pathway and inhibiting MMP-7 expression ⁽¹⁵⁾. Apoptosis in human hepatoma cells occurred via c-Jun N-terminal kinase induction ⁽¹⁶⁾ and caspase activation ⁽¹⁷⁾. Decreased adhesion of gastric cancer cells to endothelial tissue was attributed to inhibition of E-selection expression ⁽¹⁸⁾. Inhibition of tumor cell growth may also occur by stimulating cytotoxic T-lymphocyte production via IL-2 and IFN-gamma secretion ⁽¹⁹⁾. Andrographolides also enhanced doxorubicin-induced cell death in several human cancer cell lines, mainly through JAK-STAT suppression ⁽²⁰⁾.

In HIV patients, andrographolides inhibited HIV-induced cell-cycle dysregulation and increased CD4+ lymphocyte levels ⁽¹⁰⁾.