Chonbuk National University

About: Chonbuk National University is a education organization based out in Jeonju, South Korea. It is known for research contribution in the topics: Apoptosis & Nanofiber. The organization has 14820 authors who have published 28884 publications receiving 554131 citations.

Fate, occurrence, and toxicity of veterinary antibiotics in environment

Abstract: The increasing worldwide usages of Veterinary Antibiotics (VAs) for therapeutic and nontherapeutic are becoming serious issue due to its adverse effects on all living organisms. Release of VAs into the aquatic and terrestrial environments results in antibiotic resistance in bacteria and toxicity to humans, animals, and plants. This review covers the present scenario on VA usage, occurrence, toxicity, and removal techniques.

Hyaluronan inhibits osteoclast differentiation via Toll-like receptor 4.

Abstract: The differentiation of osteoclasts, cells specialized for bone resorption, is governed by two key factors, macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappaB ligand (RANKL). The extracellular matrix (ECM) is an important factor influencing cell fate. To date, little investigation on the relationship between ECM components and osteoclast differentiation has been documented. In this study, we uncovered a potent anti-osteoclastogenic effect of hyaluronan (HA), an ECM component present in bone marrow and soft connective tissues, in primary mouse and human osteoclast precursor cell cultures. The anti-osteoclastogenic function of HA was dependent on Toll-like receptor 4 (TLR4) but not on CD44. HA inhibited M-CSF-dependent signaling pathways involving Rac, reactive oxygen species and mitogen-activated protein kinases, resulting in suppression of transcription factors AP-1 and MITF that control RANK expression. Furthermore, in an in vivo mouse model of calvarial bone resorption assays HA reduced RANKL-induced bone erosion and osteoclastogenesis. Our results clearly show that HA inhibits osteoclast differentiation through TLR4 by interfering with M-CSF signaling, and point that the interaction between ECM components and innate immune receptors can play an important role in the regulation of bone metabolism.

Rosiglitazone ameliorates cisplatin-induced renal injury in mice.

Abstract: Background. Inflammatory mechanisms may play an important role in the pathogenesis of cisplatin nephrotoxicity. Agonists of the peroxisome proliferatoractivated receptor-g (PPARg), such as rosiglitazone, have been recently demonstrated to regulate inflammation by modulating the production of inflammatory mediators and adhesion molecules. The purpose of this study was to examine the protective effects of rosiglitazone on cisplatin nephrotoxicity and to explore the mechanism of its renoprotection. Methods. Mice were treated with cisplatin with or without pre-treatment with rosiglitazone. Renal functions, histological findings, aquaporin 2 (AQP2) and adhesion molecule expression, macrophage infiltration and tumour necrosis factor-a (TNF-a) levels were investigated. The effect of rosiglitazone on nuclear factor (NF)-kB activity and on viability was examined using cultured human kidney (HK-2) cells. Results. Rosiglitazone significantly decreased both the damage to renal function and histological pathology after cisplatin injection. Pre-treatment with rosiglitazone reduced the systemic levels of TNF-a and downregulated adhesion molecule expression in addition to the infiltration of inflammatory cells after cisplatin administration. Rosiglitazone restored the decreased AQP2 expression after cisplatin treatment. Pretreatment with rosiglitazone blocked the phosphorylation of the p65 subunit of NF-kB in cultured HK-2 cells. Rosiglitazone had a protective effect via a PPARg-dependent pathway in cisplatin-treated HK-2 cells. Conclusion. These results showed that pre-treatment with rosiglitazone attenuates cisplatin-induced renal damage through the suppression of TNF-a overproduction and NF-kB activation.