title: Ginsenoside Rb1 and paeoniflorin inhibit transient receptor potential vanilloid-1-activated IL-8 and PGE₂ production in a human keratinocyte cell line HaCaT.
abstract: Ginsenoside Rb1 (GRb1) and paeoniflorin (PF) are active substances of Chinese traditional herbs and have been commonly used to treat skin inflammation diseases, but little is known about the mechanisms involved. In the present study, the effects of GRb1 and PF on the production of inflammatory mediators and the possible mechanisms of transient receptor potential vanilloid-1 (TRPV1) in these mediators induction were explored. It has been shown that GRb1 and PF inhibited the productions of IL-8 and PGE₂ induced by capsaicin (CAP) in HaCaT cells and HEK 293T-TRPV1 cells (which were transgenic and overexpressed TRPV1) but had no effect on HEK 293T mock cells (p<0.05). Besides, CAP was able to induce calcium influx and nuclear factor kappa B(NF-κB) transcriptional activity in HaCaT cells and HEK 293T-TRPV1 cells, but had no effect on HEK 293T mock cells. Furthermore, GRb1 inhibited CAP-induced calcium influx and NF-κB transcriptional activity in both HaCaT cells and HEK 293T-TRPV1 cells. However, PF decreased CAP-induced calcium influx and NF-κB transcriptional activity only in HaCaT cells. This would suggest that GRb1 inhibits CAP-induced calcium influx and NF-κB activity through TRPV1 signal, while calcium influx and NF-κB activity might not be involved in the inhibitory effect of PF on TRPV1 signal. Furthermore, the inhibitory rates of GRb1 and PF on IL-8 and PGE₂ production were higher than those caused by capsazepine, an antagonist of TRPV1, suggesting that GRb1 and PF have great potential in clinical treatment of skin diseases.
authors.affiliation: Department of Pharmacy, Changhai Hospital, Second Military Medical University, 168, Changhai Road, Shanghai 200433, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Huang
authors.forename: Lei
authors.initials: L
authors.lastname: Qiu
authors.forename: Li
authors.initials: L
authors.lastname: Ding
authors.forename: Shaozhan
authors.initials: S
authors.lastname: Wang
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Quangang
authors.initials: Q
authors.lastname: Zhu
authors.forename: Fengyu
authors.initials: F
authors.lastname: Song
authors.forename: Jinhong
authors.initials: J
authors.lastname: Hu
mesh_terms: D001565:Benzoates / Q000494:pharmacology*; D001952:Bridged-Ring Compounds / Q000494:pharmacology*; D002460:Cell Line; D005786:Gene Expression Regulation; D036145:Ginsenosides / Q000494:pharmacology*; D005960:Glucosides / Q000494:pharmacology*; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism*; D015603:Keratinocytes / Q000187:drug effects* / Q000378:metabolism*; D039821:Monoterpenes; D016328:NF-kappa B / Q000378:metabolism; D050916:TRPV Cation Channels / Q000037:antagonists & inhibitors* / Q000378:metabolism; D006027:Glycosides
chemical_list: D001565:Benzoates; D001952:Bridged-Ring Compounds; D036145:Ginsenosides; D005960:Glucosides; D016209:Interleukin-8; D039821:Monoterpenes; D016328:NF-kappa B; D050916:TRPV Cation Channels; C494482:TRPV1 protein, human; C015423:peoniflorin; D006027:Glycosides; C442759:ginsenoside Rb1