Glycosides isolated from noni juice inhibit AP-1 transactivation and cell transformation in mouse epidermal JB6 cell lines ⁽²⁾. Antidiabetic characteristics of some noni compounds are attributed to inhibition of the protein tyrosine phosphatase 1B enzyme ⁽³⁵⁾. Anti-inflammatory activity in noni extract was attributed to quercetin ⁽³⁴⁾. In addition, noni juice exhibited antioxidant effects by reducing aromatic DNA adducts ^(5) (19).

In animal models, an aqueous extract of noni root produced a central analgesic effect that was antagonized by naloxone ⁽⁶⁾. Hepatoprotective effects occur through regulation of lipid homeostasis, antioxidant status, and anti-inflammatory responses ^(36) (37). The primary iridoid deacetylasperulosidic acid may exert antioxidant effects by increasing superoxide dismutase activity ⁽⁴²⁾. Scopoletin and rutin in noni may be responsible for antidopaminergic and antiadrenergic effects ⁽⁴⁶⁾. Scopoletin also stimulates gastrointestinal motility by acting as a 5-HT4 receptor agonist ⁽³⁸⁾. Treatment with noni extract prevented memory impairment through increased brain energy metabolism, cholinergic neurotransmission, brain-derived neurotrophic factor, and antioxidative activity ⁽⁴⁰⁾.

When combined with suboptimal doses of certain chemotherapy agents, polysaccharides from noni improved survival time and curative effects ⁽⁴⁾. Apoptotic effects occur via upregulation of p53 and proapoptotic Bax proteins, as well as downregulation of the antiapoptotic Bcl-2, Bcl-XL proteins and survivin. Increase in caspase 9 and 3 was also reported, which suggests involvement of the intrinsic mitochondrial pathway ⁽³¹⁾. In cervical cancer cell lines, malondialdehyde levels were significantly reduced when treated with noni, alone or in combination with cisplatin alone ⁽⁴⁴⁾. The antitumor effects of damnacanthal from noni are attributed to its inhibitory effects on the HGF/c-Met axis in human hepatocellular carcinoma cells, with decreases in Akt phosphorylation and matrix metalloproteinase-2 secretion ⁽³⁹⁾. Noni extract induced apoptosis, G1/S phase cell-cycle arrest, and decreased intracellular ROS generation and mitochondrial membrane potential in breast cancer cells ⁽⁴⁷⁾.