Skip to main content

Table 6 Main clinical application and mechanism of berberine

From: The status of and trends in the pharmacology of berberine: a bibliometric review [1985–2018]

Clinical applicationMechanismLiterature
Anti-diarrhealAntibacterial (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, 41,42,43,44]
(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
Anti-diabeticStimulation 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
(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
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
(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