Nageen Sharma
Craniosacral therapy
Faisalabad, Punjab, Pakistan
Years of experience 3

Total years in practice: 3

Published Date
December 16, 2010
Abstract Authors
Mijung Yeom, Jongbong Park, Bombi Lee, Sang-Yun Choi, Kyoung Soo Kim, Hyejung Lee, Dae-Hyun Hahm
Abstract Source
Inflamm Res. 2010 Dec 16. Epub 2010 Dec 16. PMID: 21161563
Abstract Affiliation
Department of Oriental Medicine, Acupuncture and Meridian Science Research Center, Kyung Hee University, Hoegi-dong, Dongdaemoon-gu, Seoul, 130-702, Republic of Korea.
Study Type
Research
Conditions
Arthritis, Cancer Care, Rheumatoid Arthritis
Therapies
Functional Medicine, Naturopathic Medicine
Reference
Abstract Content
OBJECTIVE:
Lactoferrin (Lf) is known to have anti-cancer and anti-inflammatory activities; however, its therapeutic mechanism has not been defined. In this study, to explain the therapeutic mechanism of Lf, we examined the effect of Lf on endothelial cell activation, leukocyte integration, and angiogenesis in vitro.
METHODS:
Endothelia-leukocyte adhesion assays were used to assess primary cultures of bovine aortic endothelial cells (BAECs) activation following LPS treatment. The mRNA expression of ICAM-1 and proinflammatory cytokines was measured using RT-PCR. Each step of angiogenesis was evaluated in vitro, including endothelial cell proliferation, migration, and tube formation. Proliferation was examined using WST-1 and BrdU incorporation assays, while wound migration assays were used to evaluate cell migration; capillary-like tube formation assays on Matrigel were used to assess tube formation.
Results:
Lf reduced the adhesion of human monocyte-like THP-1 cells to BAECs by 45%. Lf also reduced mRNA expression of ICAM-1 and proinflammatory cytokines in BAECs. Lf significantly inhibited BAEC proliferation, migration, and tube formation. CONCLUSIONS: Lf exerted a potent effect on BAEC activation, suggesting that it might function via an endothelia-based mechanism in the treatment of various s, including rheumatoid arthritis and cancer.
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