Myrrh

Anti-inflammatory: Myrrh is thought to mediate its anti-inflammatory activity through inducing haem oxygenase activity. Haem oxygenase then appears to prevent the degradation of IKBalpha in response to inflammatory receptor activation. This prevents translocation of nuclear factor kappaB (NFkappaB) to the nucleus and inhibits the expression of genes under its control like cyclooxygenase-2 and the inducible form of nitric oxide synthase. The suppression of the NFkappaB pathway likely also reduces the expression of inflammatory cytokines. Myrhh also inhibits the mitogen activated protein kinase (MAPK) pathway, specifically producing inhibition of p38 and c-jun N-terminal kinase (JNK). This is associated with a reduction in c-jun and c-fos expression which would likely result in a reduction in activator protein-1 and and inhibition of its associated inflammatory gene expression. Myrrh exibits inhibitory activity against 5-lipoxygenase helping to suppress the production of leukotrienes, another class of inflammatory cytokine. In addition to its effects on the NFkappaB system, myrrh also inhibits the signal transducer and activator of transcription (STAT) -1 and -3 resulting in a decrease in cytokine production by the janus kinase/STAT pathway. Myrrh also reduces the downregulation of suppresor of cytokine synthesis (SOCS) in response to interleukin-1beta and interferon-gamma. SOCS serves as an autoregulator of the JAK/STAT pathway under transcriptional control of STATs and inhibits activation of the pathway.

Analgesic: Myrrh appears to produce an analgesic effect associated with its suppression of prostaglandin production. Myrrh is also suggested to block inward sodium currents.

Anticancer: Myrrh displays an pro-apoptotic effect on cancer cells. This seems to involve members of the Bcl family of proteins. Myrrh induces the expression of the pro-apoptotic protein Bax while decreasing the expression of Bcl-2 and Bcl-xl, the anti-apoptotic members of the Bcl family. At low doses Myrrh seems to activate the MAPK pathway in cancer cells, promoting the phosphorylation of p38 and JNK. The JNK activation in particular appears to mediate an apoptotic influence. Additionally, myrrh appears to induce reactive oxygen species generation in cancer cells further promoting apoptosis.

Antibacterial/Antiparasitic/Antifungal: The precise antibacterial, antiparasitic, and antifungal mechanisms of myrrh are unknown.

Hepatoprotective: Myrrh has been shown to reduce liver injury and upregulation of superoxide dismutase, glutathione peroxidase and catalase in response to carbon tetrachloride insult. This is thought to be due to anti-oxidant properties of myrrh.

Antioxidant: The precise mechanism of myrrh's antioxidant property is unknown.

Lipid lowering: Compounds in myrrh bind to and inhibit the farnesoid X receptor resulting in a reduction in low density lipoprotein. This effect is likely to due the attenuation of the suppression of bile synthesis and a reduction in ileal bile acid binding protein in response to farnesoid X receptor stimulation. Together these would ensure processing of cholesterol into bile and subsequent loss of that bile by reducing reuptake.

Cardioprotective: The exact mechanism of myrrh's cardioprotective effect is unknown.

Antidiabetic: Much of myrrh's antidiabetic action is attrbutable to it's anti-inflammatory action which protects islet beta cells from inflammatory damage during hyperglycemia. The antioxidant properties of myrrh also likely contribute to this effect.

Antiulcer: The antiulcer activity of myrrh is suggested to be due to inhibition of gastric acid secretion, increasing gastric mucus secretion, and myrrh's antioxidant properties.