Resiniferatoxin ((+)-Resiniferatoxin) is a highly potent synthetic TRPV1 agonist that inhibits the production of Th1 cytokines and has anti-inflammatory activity, reducing serum levels of IL-12, INF-γ, IL-1β, TNF-α, NO, and PGE.

METHODS: RAW264.7 cells were treated with LPS (100 ng/ml) and IFN-γ (3 ng ml−1) and then treated with Resiniferatoxin ((+)-Resiniferatoxin) (0.01, 0.1, 1, 10.24 h). The culture medium was collected for NO determination, and the cell lysates were subjected to SDS-PAGE to measure and quantify iNOS or COX-2 immunoreactivity.
RESULTS At a concentration of 10 μM, Resiniferatoxin ((+)-Resiniferatoxin) inhibited LPS-induced NO production by 67±10% and 52±6%, respectively, and failed to affect LPS-induced COX-2 and PGE2 responses. [3]

METHODS: Resiniferatoxin ((+)-Resiniferatoxin) (2 μg/10 μl) was injected intrathecally into the T2/T3 space of mice. Cardiac sympathetic nerve activity (CSNA) and cardiac electrophysiology were assessed two weeks later.
RESULTS Intrathecal injection of Resiniferatoxin ((+)-Resiniferatoxin) significantly and selectively eliminated the expression of dorsal horn afferent markers (TRPV1 and calcitonin gene-related peptide) and reduced overactive CSNA. Electrophysiological studies have shown that intrathecal administration of Resiniferatoxin ((+)-Resiniferatoxin) can significantly reverse the prolongation of action potential duration (APD) and APD alternating hormones and reduce the inducibility of ventricular arrhythmias. [4]