Bong-Seok Kang

Anti-Inflammatory Effect of Ascochlorin in LPS-Stimulated RAW 264.7 Macrophage Cells Is Accompanied With the Down-Regulation of iNOS, COX-2 and Proinflammatory Cytokines Through NF-κB, ERK1/2, and p38 Signaling Pathway

A natural compound C23H32O4Cl, ascochlorin (ASC) isolated from an incomplete fungus, Ascochyta viciae has been known to have several biological activities as an antibiotic, antifungal, anti‐cancer, anti‐hypolipidemic, and anti‐hypertension agent. In this study, anti‐inflammatory activity has been investigated in lipopolysaccharide (LPS)‐induced murine macrophage RAW 264.7 cells, since ASC has not been observed on the inflammatory events. The present study has clearly shown that ASC (1–50 μM) significantly suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2) and decreased the gene expression of inducible NO synthase (iNOS) and cyclooxygenase‐2 (COX‐2) in a dose‐dependent manner. Moreover, ASC inhibited the mRNA expression and the protein secretion of interleukin (IL)‐1β and IL‐6 but not tumor necrosis factor (TNF)‐α in LPS‐stimulated RAW 264.7 macrophage cells. In addition, ASC suppressed nuclear translocation and DNA binding affinity of nuclear factor‐κB (NF‐κB). Furthermore, ASC down‐regulated phospho‐extracellular signal‐regulated kinase 1/2 (p‐ERK1/2) and p‐p38. These results demonstrate that ASC exhibits anti‐inflammatory effects in RAW 264.7 macrophage cells. J. Cell. Biochem. 117: 978–987, 2016.

Interleukin-1 and tumor necrosis factor-α induce collagenolysis and bone resorption by regulation of matrix metalloproteinase-2 in mouse calvarial bone cells

Abstract Interleukin‐1β (IL‐1β) and tumor necrosis factor‐α (TNF‐α) greatly induces osteoclast formation and stimulates bone resorption of mouse calvaria in culture. We examined the effects of the two cytokines on the collagenolysis and bone resorption by induction of matrix metalloproteinases (MMPs). The cells were analyzed using zymographic analysis. It was shown that the mouse calvarial osteoblasts constitutively synthesize progelatinase‐A (MMP‐2). Interleukin‐1β markedly enhanced the messenger RNAs (mRNAs) expression of MMP‐2 (gelatinase A), but slightly MMP‐9 (gelatinase B), which associated with increases in bone matrix degradation. Both pro‐ and active‐forms of MMP‐2 were detected in the conditioned medium collected from calvarial cultures, and IL‐1β markedly stimulated both pro‐ and active‐forms of the MMP‐2. The expression of MMP‐2 mRNAs could be detected, and they were markedly enhanced by IL‐1β on days 1 and 2. These results demonstrate that the potency of induction of MMP‐2 by IL‐1β and TNF‐α is closely linked to the respective bone‐resorbing activity, suggesting that MMP‐2‐dependent degradation of bone matrix plays a key role in bone resorption induced by these cytokines. On the other hand, when the mouse osteoblasts were stimulated with parathyroid hormone, 1,25(OH)2D3, mononuclear cell conditioned medium (MCM) and IL‐1 as bone resorption agents, collagenolysis was increased by producing the active gelatinase. Interleukin‐1 in stimulating bone resorption was examined using fetal mouse long bone organ culture. Interleukin‐1 stimulated bone resorption and produced marked resorption when present simultaneously. Furthermore, treatment of indomethacin and dexamethasone clearly abolished the responses of IL‐1α and IL‐1β.

Effects of TGFβ1 and extracts from Cervus korean TEMMINCK var. mantchuricus Swinhoe on acute and chronic arthritis in rats

AIM OF THE STUDY To elucidate the pharmacological activities of deer antler acupuncture and TGF61538;1 on the acute and chronic phases of rheumatoid arthritis diseases. MATERIALS AND METHODS Polyarthritis rats were administered with TGF61538;1 and water extract of deer antler acupunture (DAA), prepared from the pilose antler of Cervus korean TEMMINCK var. mantchuricus Swinhoe. TGF61538; (0.1 to 2 61549;g/animal) and DAA (5-100 61549;g/kg animal) were initiated 1 day before an arthritogenic dose of streptococcal cell wall fragments to see the effects on the joint swelling and distortion during the acute phase and the chronic phase of the disease. Arthritic index suppression of rat arthritis model was examined by TGF61538; and DAA administrations. RESULTS TGF61538;1 and DAA diminished the polyarthritis development in rats. TGF61538; and DAA eliminated the joint swelling and distortion observed during the acute phase and the chronic phase of the disease. The TGF61538; and DAA suppressed the arthritis progress when administration was begun after acute phase of arthritis. DISCUSSION Consistent with the inhibition of inflammatory cell recruitment into the synovium, TGF61538;1 and DAA reversed the leukocytosis associated with the chronic phase of the arthritis, respectively.

IL‐1β Induces and TGF‐β Reduces Vitamin D3‐Induced Bone Resorption in Mouse Calvarial Bone Cells

Bone cells produce multiple growth factors and cytokines that have effects on bone metabolism and can be incorporated into the bone matrix. The present study was designed to extend these observations by examining the interactions between transforming growth factor‐β (TGF‐β) or interleukin‐1β (IL‐1β) and bone cells in a rat long bone culture model. IL‐1β regulates several activities of the osteoblast cells derived from rat long bone explants in vitro. IL‐1β stimulated cellular proliferation and the synthesis of prostaglandin E2 and plasminogen activator activity in the cultured cells in a dose‐dependent manner. TGF‐β is present in the bone matrix and potentially can be released during bone resorption. TGF‐β reduced basal bone resorption and inhibited vitamin D3 [1,25(OH)2D3]‐induced bone resorption in rat long bone cells. These studies support the role of IL‐1β in the pathological modulation of bone cell metabolism, with regard to implication in the pathogenesis of osteoporosis by IL‐1β, and that TGF‐β is positively inhibiting the bone resorption.

Induction of a TC1-mediated experimental autoimmune thyroiditis by deglycosylated porcine thyroglobulin.

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