The present study was to evaluate the effects of Achyranthes japonica Nakai(AJ), Achyranthes bidentata Blume(AB), Cyathula officinalis Kuam(CO) and Cyathula capitata Moquin(CC) on inflammation. In LPS-stimulated RAW 264.7 macrophages, AJ extract significantly inhibited productions of nitric oxide(NO...
The present study was to evaluate the effects of Achyranthes japonica Nakai(AJ), Achyranthes bidentata Blume(AB), Cyathula officinalis Kuam(CO) and Cyathula capitata Moquin(CC) on inflammation. In LPS-stimulated RAW 264.7 macrophages, AJ extract significantly inhibited productions of nitric oxide(NO) and interleukine-1beta(IL-1β) compared with other extracts. In addition, AJ extract reduced secretion of prostaglandin E2(PGE2), and tumor necrosis factor-alpha(TNF-α), and suppressed the expression of inducible nitric oxide synthase(iNOS) and cyclooxygenase-2(COX-2) proteins as well as matrix metalloproteinase-9 (MMP-9) activity in LPS-treated RAW 264.7 cells. Furthermore, we investigated the effects of AJ extract on immune reaction and osteoclast formation closely associated with rheumatoid arthritis. AJ extract dose-dependently inhibited type II collagen-stimulated DNA synthesis and LPS-induced production of IL-1β in spleen cells derived from type II collagen-immunized mice. In contrast, AJ extract alone induced TNF-α production. Moreover, we found that AJ, AB, CO and CC extracts at nontoxic doses reduced RANKL-induced osteoclast formation in bone marrow macrophages(BMMs). Based on these in vitro data, we confirmed the effects of AJ on acute and chronic inflammation using animal models. 12-O-tetradecanoylphorbol 13-acetate(TPA)-induced ear edema was inhibited by pretreatment with AJ extract and chloroform and water fractions in mice. However, arthritis score and paw thickness did not suppress by treatment with AJ extract in mice with type II collagen athritis (CIA), characterized chronic inflammation of multiple joints and destruction of cartilage and bone. Taken together, AJ extract has better anti-inflammatory activity than AB, CO and CC extracts. AJ extract may inhibit acute inflammation, not chronic inflammation such as rheumatoid arthritis, by blocking production of NO, PGE2 and proinflammatory cytokines in LPS-stimulated macrophages.
The present study was to evaluate the effects of Achyranthes japonica Nakai(AJ), Achyranthes bidentata Blume(AB), Cyathula officinalis Kuam(CO) and Cyathula capitata Moquin(CC) on inflammation. In LPS-stimulated RAW 264.7 macrophages, AJ extract significantly inhibited productions of nitric oxide(NO) and interleukine-1beta(IL-1β) compared with other extracts. In addition, AJ extract reduced secretion of prostaglandin E2(PGE2), and tumor necrosis factor-alpha(TNF-α), and suppressed the expression of inducible nitric oxide synthase(iNOS) and cyclooxygenase-2(COX-2) proteins as well as matrix metalloproteinase-9 (MMP-9) activity in LPS-treated RAW 264.7 cells. Furthermore, we investigated the effects of AJ extract on immune reaction and osteoclast formation closely associated with rheumatoid arthritis. AJ extract dose-dependently inhibited type II collagen-stimulated DNA synthesis and LPS-induced production of IL-1β in spleen cells derived from type II collagen-immunized mice. In contrast, AJ extract alone induced TNF-α production. Moreover, we found that AJ, AB, CO and CC extracts at nontoxic doses reduced RANKL-induced osteoclast formation in bone marrow macrophages(BMMs). Based on these in vitro data, we confirmed the effects of AJ on acute and chronic inflammation using animal models. 12-O-tetradecanoylphorbol 13-acetate(TPA)-induced ear edema was inhibited by pretreatment with AJ extract and chloroform and water fractions in mice. However, arthritis score and paw thickness did not suppress by treatment with AJ extract in mice with type II collagen athritis (CIA), characterized chronic inflammation of multiple joints and destruction of cartilage and bone. Taken together, AJ extract has better anti-inflammatory activity than AB, CO and CC extracts. AJ extract may inhibit acute inflammation, not chronic inflammation such as rheumatoid arthritis, by blocking production of NO, PGE2 and proinflammatory cytokines in LPS-stimulated macrophages.
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