Publications by authors named "C Chanbora"

Objectives: Lactoferrin (LF) possesses diverse biological functions. We previously reported that bovine LF (bLF) attenuates lipopolysaccharide-induced bone resorption in osteoblasts. In addition to its ability to inhibit osteoclastogenesis, bLF has been implicated in stimulating bone formation.

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Background: Vascular endothelial growth factor (VEGF) is a highly specific signaling protein for vascular endothelial cells that plays a critical role in tumor growth and invasion through angiogenesis, and may contribute to cell migration and activation of pre-osteoclasts, osteoclasts and some tumor cells.

Objectives: We aimed to clarify the detailed roles of VEGF-Flt-1 signaling in bone invasion of oral squamous cell carcinoma (OSCC) cells.

Results: Forty-two (42) of 54 cases with gingival SCC (77.

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There is an urgent clinical need for an effective therapeutic agent to treat neuropathic pain. This study explored whether intrathecal administration of bovine lactoferrin (bLF), in combination with signal transduction pathway inhibition or an inflammatory cytokine production, results in reduced allodynia/hyperalgesia in the whisker pad area following mental nerve transection (MNT) in rats. Rats were intrathecally infused with bLF, lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS), an antagonist of Toll-like receptor 4 (TLR4), or interleukin (IL)-18 binding protein (BP).

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Background: Cholestatic liver diseases exhibit higher levels of serum γ-glutamyl transpeptidase (GGT) and incidence of secondary osteoporosis. GGT has been identified as a novel bone-resorbing factor that stimulates osteoclast formation. The aim of this study was to elucidate the interaction of elevated GGT levels and cholestatic liver disease-induced bone loss.

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Background: Control of periodontal tissue inflammation during orthodontic treatment is very important in achieving a favourable therapeutic goal. We previously demonstrated that orally applied bovine lactoferrin (bLF) inhibited LPS-induced bone resorption but not orthodontic force-induced tooth movement in vivo. This study is designed to examine the underlying mechanism of it.

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