Table 6.
Clinical application | Mechanism | Literature |
---|---|---|
Anti-diarrheal |
Antibacterial (e.g., Vibrio cholerae) Inhibition of intestinal smooth muscle movement regulates intestinal motility Inhibition of intestinal mucosa K+’s influx restores intestinal barrier function |
[10, 41–44] |
Anticancer (cancer arising from leucocytes, liver, lung, stomach, colon, skin, oral, etc.) |
Chemical carcinogenic protection Independent of the mevalonate pathway Directly induces apoptosis Downregulation of nuclear transcription factors Exertion of indirect effects Suppression of DNA |
[45–54] |
Anti-diabetic |
Stimulation of AMPK activity and might inhibit PPARγ activity Promotion of the proliferation of 3T3-L1 pre-adipocytes, reduced lipid accumulation, and inhibition of their differentiation Insulinotropic effects Good action for lipid metabolism Targeting of non-coding RNAs Promotion the expression of GLUT1 Modulation of the gut microbiota |
[55–61] |
Anti-cardiovascular (e.g., Atherosclerosis) |
Inhibition of the expression of LOX-1 through ET-1 receptors Impacts on potassium ion channels (K +) Increased NO and cGMP content Blockage of K + channels sensitive to ATP and voltage Inhibition of mitogen-activated kinase/extracellular signals |
[62–65] |
Anti-inflammatory and immune regulation (e.g., ulcerative colitis) |
Inhibit cox-2, AP-1 binding Downregulation of activation of ERK 1/2 and p38 signallings pathways, Inhibition of the production of pro-inflammatory factors Downregulation of p-ERK, p-p38, and p-JNK activation Inhibition of the expression of monocyte chemoattractant protein 1 and cytokine-induced neutrophil chemoattractant 1 induced by lipopolysaccharide Inhibition of RNA virus reverse transcriptase activity Inhibition of the synthesis of anti-SRBC antibodies Reduced content of PGF2a in inflammatory tissues |
[66–72] |
Antipsychotic (e.g., depression, Alzheimer’s,) |
Increased NE and 5-HT concentrations in the brain Promotion of axon extension and axon regeneration in PNS-damaged nerves Increased expression of BDNF mRNA in the hippocampus Actions on the pathological process of amyloid Aβ, inhibitings glial proliferation Inhibition of tau hyperphosphorylation induced by calmodulin A and its induced cytotoxicity Inhibition of MAO activity |
[73–78] |