Phytol – Terpenes and Cannabinoid Research

Phytol Properties and Effects

Phytol is associated with the following properties and effects:

1. Anti-diabetic
   
   
   
   1. Improves glucose tolerance (H. Upadhyay et al., 2022)
   
   
   
   


2. Anti-microbial
   
   
   
   1. Anti-parasitical (against Plasmodium berghei) (M. Usman et al., 2022) 
   
   
   
   


3. Anti-obesity (Ji-Yeong An et al., 2018)

Anti-inflammatory and antioxidant (via regulation of NF- κB and AP-1 activation, inhibits levels of IL-1β, IL-4, and TNF- α, neutrophil migration, reduces reactive oxygen species and reactive nitrogen species level by activating antioxidative defense system (Superoxide dismutase and catalase) and restoring Glutathione S-transferase)

Anticonvulsant, anxiolytic, sedative, and neuroprotective properties (via possible activities on GABA receptors, anticholinesterase, butyrylcholinesterase, β-secretase 1 (BACE1), attenuating macromolecular damage, antioxidant activities, and regulating apoptosis-mediated cell death)

Antimicrobial against Staphylococcus aureus and Pseudomonas aeruginosa (via inducing oxidative stress response in P. aeruginosa and damage to the cell membranes with bactericidal activity against S. aureus)

Anti-parasitical against schistosomiasis and Plasmodium berghei (via reducing worm burden, egg laying, suppresses parasitemia, reduces anemia, and oxidative brain damage in test animals infected with Plasmodium berghei)

A potential antihyperglycemic and antiobesity agent may improve oral glucose tolerance and increase brown adipocytes (via PPAR-α and -γ binding)

Pain-reducing (via central and peripheral actions, antioxidant properties)

Anticancer and anti-drug resistance activities. It may help destroy some types of adenocarcinoma, hepatocellular, lung, and skin epidermal cancer cells in vitro and ex-vivo.

It prevents drug resistance in AML models. However, it may also cause selective midzonal hepatocellular necrosis in mice (via apoptosis induction through activation of caspase-9/3 and inhibition of EMT in hepatocellular carcinoma cells, apoptosis in human gastric adenocarcinoma AGS cells through downregulation of Bcl-2, upregulation of Bax, the activation of caspase-9 and -3, PARP cleavage, and depolarization of the mitochondrial membrane, suppresses the P-gp expression via NF-κB inhibition in AML, interactions with β-C, AO-(2) and P may cause induction of apoptosis on A431 and HaCaT cells, antioxidant activities)

Last reviewed by Dr. Abraham Benavides, M.D., 05-27-2022