Employing a PAR1-activating peptide, TFLLR-NH2, and its receptor-inactive reverse-sequence peptide, RLLFT-NH2, along with experiments done in PAR1-null mice, we established not only that (1) PAR1 can play an anti-inflammatory role in noninfectious prostatitis by elevating the anti-inflammatory cytokine IL-10 and diminishing swelling but also that (2) the PAR1-activating peptide (but not its reverse-sequence agonist) can, via a non-PAR1 mechanism, exhibit substantial anti-inflammatory actions. Here, IL10 is linked to prostatitis.