4-Hexylresorcinol: pharmacologic chaperone and its application for wound healing

Abstract

Abstract4-Hexylresorcinol (4HR) is amphiphilic organic chemical and auto-regulator for micro-organism. As 4HR administration induces the stress on the endoplasmic reticulum, 4HR changes protein folding. The application of 4HR inhibits NF-κB signal pathway and TNF-α production. In addition, 4HR administration increases VEGF, TGF-β1, and calcification associated proteins. As a consequence, 4HR administration increases angiogenesis and bone formation in wounded area. Strong anti-inflammatory reaction and capillary regeneration in diabetic model demonstrate that 4HR can be applied on many types of surgical wound.

Administration of 4‑hexylresorcinol increases p53‑mediated transcriptional activity in oral cancer cells with the p53 mutation

“…The administration of 4HR decreases the expression level of HDAC4 in HUVECs ( 18 ) and Saos-2 cells ( 37 ). 4HR is a chemical chaperone ( 16 ) that increases the stress of the ER, which may be induced by changes in protein folding ( 38 ). Thus, investigation of acetylation and phosphorylation of p53 would be interesting topic.…”

“…This is a combined action of ER stress and HDAC inhibition (16,20). When 4HR is provided to microorganisms with mutant enzymes, the enzyme activity is recovered by 4HR administration (16). The administration of 4HR to KB cells shows an anticancer effect, but KB cells have wild-type p53 (21)(22)(23).…”

“…Therefore, chemicals that can change mutant p53 conformation and have antioxidant properties should be investigated. 4-Hexylresorcinol (4HR) is a chemical chaperone that has antioxidant properties ( 16 , 17 ) and is an histone deacetylase (HDAC) inhibitor ( 18 ). The administration of 4HR induces endoplasmic reticulum (ER)-mediated stress potentially by protein folding changes ( 16 ).…”

“…4-Hexylresorcinol (4HR) is a chemical chaperone that has antioxidant properties ( 16 , 17 ) and is an histone deacetylase (HDAC) inhibitor ( 18 ). The administration of 4HR induces endoplasmic reticulum (ER)-mediated stress potentially by protein folding changes ( 16 ). When 4HR is administered to HUVECs, the expression level of transforming growth factor-β1 (TGF-β1) is increased ( 19 ).…”

“…When 4HR is administered to HUVECs, the expression level of transforming growth factor-β1 (TGF-β1) is increased ( 19 ). This is a combined action of ER stress and HDAC inhibition ( 16 , 20 ). When 4HR is provided to microorganisms with mutant enzymes, the enzyme activity is recovered by 4HR administration ( 16 ).…”