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3 results on '"Jong-Hwei S. Pang"'

1. The Anti-Atherosclerotic Effect of Naringin Is Associated with Reduced Expressions of Cell Adhesion Molecules and Chemokines through NF-κB Pathway

Author

Tun-Pin Hsueh, Jer-Ming Sheen, Jong-Hwei S. Pang, Kuo-Wei Bi, Chao-Chun Huang, Hsiao-Ting Wu, and Sheng-Teng Huang

Subjects
naringin, atherosclerosis, TNF-α, chemokines, NF-κB, Organic chemistry, QD241-441
Abstract

Naringin has been reported to have an anti-atherosclerosis effect but the underlying mechanism is not fully understood. The aim of this study is to investigate the impact of naringin on the TNF-α-induced expressions of cell adhesion molecules, chemokines and NF-κB signaling pathway in human umbilical vein endothelial cells (HUVECs). The experiments revealed that naringin, at concentrations without cytotoxicity, dose-dependently inhibited the adhesion of THP-1 monocytes to the TNF-α-stimulated HUVECs. The TNF-α-induced expressions of cell adhesion molecules, including VCAM-1, ICAM-1 and E-selectin, at both the mRNA and protein levels, were significantly suppressed by naringin in a dose dependent manner. In addition, the TNF-α-induced mRNA and protein levels of chemokines, including fractalkine/CX3CL1, MCP-1 and RANTES, were also reduced by naringin. Naringin significantly inhibited TNF-α-induced nuclear translocation of NF-κB, which resulted from the inhibited phosphorylation of IKKα/β, IκB-α and NF-κB. Altogether, we proposed that naringin modulated TNF-α-induced expressions of cell adhesion molecules and chemokines through the inhibition of TNF-α-induced activation of IKK/NF-κB signaling pathway to exert the anti-atherosclerotic effect.

Published
2016
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2. Pentadecapeptide BPC 157 Enhances the Growth Hormone Receptor Expression in Tendon Fibroblasts

Author

Wen-Chung Tsai, Chung-Hsun Chang, Ya-Hui Hsu, and Jong-Hwei S. Pang

Subjects
Male, medicine.medical_specialty, tendon fibroblast, proliferation, Pharmaceutical Science, Growth hormone receptor, Biology, Achilles Tendon, Article, Analytical Chemistry, BPC 157, Rats, Sprague-Dawley, lcsh:QD241-441, lcsh:Organic chemistry, Proliferating Cell Nuclear Antigen, Internal medicine, Drug Discovery, medicine, Animals, PCNA, Physical and Theoretical Chemistry, Receptor, Cell Proliferation, Wound Healing, Achilles tendon, Janus kinase 2, Cell growth, Organic Chemistry, Proteins, Receptors, Somatotropin, Fibroblasts, Janus Kinase 2, musculoskeletal system, Peptide Fragments, Rats, Tendon, Endocrinology, medicine.anatomical_structure, Chemistry (miscellaneous), growth hormone receptor, Growth Hormone, biology.protein, Molecular Medicine, Signal transduction, Wound healing, Signal Transduction
Abstract

BPC 157, a pentadecapeptide derived from human gastric juice, has been demonstrated to promote the healing of different tissues, including skin, muscle, bone, ligament and tendon in many animal studies. However, the underlying mechanism has not been fully clarified. The present study aimed to explore the effect of BPC 157 on tendon fibroblasts isolated from Achilles tendon of male Sprague-Dawley rat. From the result of cDNA microarray analysis, growth hormone receptor was revealed as one of the most abundantly up-regulated genes in tendon fibroblasts by BPC 157. BPC 157 dose- and time-dependently increased the expression of growth hormone receptor in tendon fibroblasts at both the mRNA and protein levels as measured by RT/real-time PCR and Western blot, respectively. The addition of growth hormone to BPC 157-treated tendon fibroblasts dose- and time-dependently increased the cell proliferation as determined by MTT assay and PCNA expression by RT/real-time PCR. Janus kinase 2, the downstream signal pathway of growth hormone receptor, was activated time-dependently by stimulating the BPC 157-treated tendon fibroblasts with growth hormone. In conclusion, the BPC 157-induced increase of growth hormone receptor in tendon fibroblasts may potentiate the proliferation-promoting effect of growth hormone and contribute to the healing of tendon.

Published
2014

3. The Anti-Atherosclerotic Effect of Naringin Is Associated with Reduced Expressions of Cell Adhesion Molecules and Chemokines through NF-κB Pathway

Author

Hsiao-Ting Wu, Tun-Pin Hsueh, Kuo-Wei Bi, Jer-Ming Sheen, Chao-Chun Huang, Jong-Hwei S. Pang, and Sheng-Teng Huang

Subjects
0301 basic medicine, Chemokine, Active Transport, Cell Nucleus, Pharmaceutical Science, Gene Expression, chemokines, IκB kinase, Article, NF-κB, Analytical Chemistry, lcsh:QD241-441, 03 medical and health sciences, chemistry.chemical_compound, lcsh:Organic chemistry, naringin, atherosclerosis, TNF-α, Drug Discovery, Cell Adhesion, Human Umbilical Vein Endothelial Cells, Humans, Physical and Theoretical Chemistry, CX3CL1, Naringin, Cells, Cultured, biology, Chemistry, Cell adhesion molecule, Tumor Necrosis Factor-alpha, Organic Chemistry, NF-kappa B, Coculture Techniques, Cell biology, 030104 developmental biology, Biochemistry, Chemistry (miscellaneous), Flavanones, biology.protein, Molecular Medicine, Phosphorylation, Signal transduction, Cell Adhesion Molecules, Signal Transduction
Abstract

Naringin has been reported to have an anti-atherosclerosis effect but the underlying mechanism is not fully understood. The aim of this study is to investigate the impact of naringin on the TNF-α-induced expressions of cell adhesion molecules, chemokines and NF-κB signaling pathway in human umbilical vein endothelial cells (HUVECs). The experiments revealed that naringin, at concentrations without cytotoxicity, dose-dependently inhibited the adhesion of THP-1 monocytes to the TNF-α-stimulated HUVECs. The TNF-α-induced expressions of cell adhesion molecules, including VCAM-1, ICAM-1 and E-selectin, at both the mRNA and protein levels, were significantly suppressed by naringin in a dose dependent manner. In addition, the TNF-α-induced mRNA and protein levels of chemokines, including fractalkine/CX3CL1, MCP-1 and RANTES, were also reduced by naringin. Naringin significantly inhibited TNF-α-induced nuclear translocation of NF-κB, which resulted from the inhibited phosphorylation of IKKα/β, IκB-α and NF-κB. Altogether, we proposed that naringin modulated TNF-α-induced expressions of cell adhesion molecules and chemokines through the inhibition of TNF-α-induced activation of IKK/NF-κB signaling pathway to exert the anti-atherosclerotic effect.

Published
2016

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