Xia-Bai-San inhibits lipopolysaccharide-induced activation of intercellular adhesion molecule-1 and nuclear factor-kappa B in human lung cells

SummaryThe cellular phospholipid, lysophosphatidic acid (LPA), released by activated platelets and fibroblasts or, at high levels, from ovarian and cervical carcinomas is a powerful serum mitogen that may modulate several signaling pathways in endothelial cells (EC). Hence, LPA could function in a paracrine manner during EC-platelet interactions at sites of vascular injury.Here, we demonstrate activation of the transcription factor nuclear factor kappa B (NF-κB) in EC following exposure to LPA. EC activation was further characterized by increased levels of mRNA transcripts encoding E-selectin, Intercellular Adhesion Molecule-1, Interleukin-8 and Monocyte Chemoattractant Protein-1. These effects were inhibited by preincubating EC either in the presence of mepacrine (to block phospholipase A2) or of pertussis toxin (to increase ADP-ribosylation of Gi proteins). No inhibition was observed in the presence of putative LPA receptor antagonists suramin or thrombospondin.LPA induces a proinflammatory activation of endothelial cells that (i) involves Gi proteins; (ii) depends on phospholipase A2 activity; (iii) is associated with the activation of NF-κB and (iv) results in increased expression of proinflammatory genes. We propose that LPA release by activated platelets may directly modulate vascular inflammatory responses. Abbreviations: EC, endothelial cells; LPA, lysophosphatidic acid; NF-κB, nuclear factor kappa B; PA, phosphatidic acid; IL-8, interleukin-8; MCP-1, monocyte chemoattractant protein-1, ICAM-1, intercellular adhesion molecule-1, vascular adhesion molecule-1; GAPDH, glycerol aldehyde phosphate dehydrogenase; MAPK, mitogen activated kinase, MEK, MAPK kinase, PAEC, porcine aortic EC.

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S-Allylcysteine as an Inhibitor of Benzo(a)pyrene-Induced Precancerous Carcinogenesis in Human Lung Cells via Inhibiting Activation of Nuclear Factor-Kappa B

Natural Product Communications ◽

10.1177/1934578x19896915 ◽

2019 ◽

Vol 14 (12) ◽

pp. 1934578X1989691

Author(s):

Kaiming Wang ◽

Qiuchen Qi ◽

Fang Zhang ◽

Yongchun Zhang ◽

Min Yang ◽

...

Keyword(s):

Cell Proliferation ◽

Nuclear Factor Kappa B ◽

Human Lung ◽

Water Soluble ◽

Human Lung Cancer ◽

Lung Cells ◽

Organosulfur Compounds ◽

Nuclear Factor ◽

Nuclear Factor Kappa ◽

Human Lung Cells

Oil-soluble organosulfur compounds in garlic are known for the anticancer effect. However, there are limited experimental studies to describe the effect of S-allylcysteine (SAC), a main water-soluble derivative of garlic, in carcinogenesis. This study investigates the prevention function of SAC on carcinogen benzo(a)pyrene (B(a)P)-induced precancerous activity in human lung cells (A549). A549 cells were either pretreated (PreTM) or concurrently treated (CoTM) with 1 μM B(a)P and either 10 or 50 μM SAC. The 50 μM CoTM group inhibited B(a)P-induced cell proliferation by approximately 100%. The 50 μM SAC CoTM and PreTM inhibited the B(a)P-induced G2/M phase shift by 119% and 100%, respectively. Furthermore, the SAC PreTM exhibited the potential to reduce the generation of reactive oxygen species (ROS) in cells relative to the B(a)P group by approximately 100%. The CoTM and PreTM elevated superoxide dismutase (SOD) by at least 70% compared with B(a)P group. In this study, we demonstrated that the mechanisms involved in the inhibitory role of SAC in B(a)P-induced carcinogenesis, including suppression of cell proliferation and DNA damage, cell cycle regulation, attenuation of ROS formation, increase of SOD activity, and inhibition of nuclear factor-kappa B (NF-κB) activity, which indicated that SAC is potentially a novel therapeutic candidate for the prevention and treatment of B(a)P-induced human lung cancer.

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CD40-CD40 ligand signal induces the intercellular adhesion molecule-1 expression through nuclear factor-kappa B p50 in cultured salivary gland epithelial cells from patients with Sjögren's syndrome

Modern Rheumatology ◽

10.3109/s10165-006-0538-7 ◽

2007 ◽

Vol 17 (1) ◽

pp. 45-53 ◽

Cited By ~ 4

Author(s):

Miwako Saito ◽

Yasuhiro Ota ◽

Hiroyuki Ohashi ◽

Yoshiaki Dei ◽

Kumiko Shimoyama ◽

...

Keyword(s):

Salivary Gland ◽

Epithelial Cells ◽

Adhesion Molecule ◽

Nuclear Factor Kappa B ◽

Cd40 Ligand ◽

Intercellular Adhesion ◽

Intercellular Adhesion Molecule ◽

Nuclear Factor ◽

Intercellular Adhesion Molecule 1 ◽

Salivary Gland Epithelial Cells

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Artesunate-tinospora combination treatment decreases nuclear factor kappa-B and intercellular adhesion molecule-1 expression in mouse malarial models

Zinc supplementation improves heme biosynthesis in rats exposed to lead ◽

10.18051/univmed.2016.v35.222-228 ◽

2016 ◽

Vol 35 (3) ◽

pp. 222 ◽

Cited By ~ 1

Author(s):

Nur Izzati ◽

Loeki Enggar Fitri ◽

Mochammad Dalhar

Keyword(s):

Adhesion Molecule ◽

Combination Treatment ◽

Nuclear Factor Kappa B ◽

Intercellular Adhesion ◽

Intercellular Adhesion Molecule ◽

Control Group ◽

Nuclear Factor ◽

Intercellular Adhesion Molecule 1 ◽

Treatment Groups ◽

The Brain

Background Cerebral malaria is a severe form of malaria caused by brain ischemia. Artesunate, an artemisinin derivative, is the standard WHO therapy for severe malaria. Tinospora crispa (brotowali) is a traditional plant with antiinflammatory, antioxidant and antiparasitic properties. The aim of this study was to determine the effect of combinations of artesunate and T. crispa extract on nuclear factor kappa-B (NFêB) and intercellular adhesion molecule-1 (ICAM-1) expression in the brain of mouse malaria models. Methods This was an experimental post-test only control group study using C57BL/6J mice infected with Plasmodium berghei, divided into 7 groups: negative control, positive control, group receiving artesunate 32 mg/kgBW, group receiving tinospora extract 3.5 mg/kgBW, and three groups receiving combinations of artesunate 32 mg/kgBW and tinospora extract 2.5 mg/kgBW, 3 mg/kgBW and 3.5 mg/BW, respectively. The expression of NFêB and ICAM-1 was measured by immunohistochemistry. One-way ANOVA was used to analyze the data. Results NFkB and ICAM-1 expression increased significantly in the positive controls compared to all other groups (p=0.000). NFkB expression was significantly lower in the groups receiving artesunate and tinospora at 3 mg/kgBW and 3.5 mg/kgBW, as compared with the artesunate only group (p=0.003; p=0.005) and the tinospora extract only group (p=0.001; p=0.003). NFkB expression in all combination treatment groups was similar to that in the negative controls (p>0.05), whereas ICAM-1 expression did not differ between single and combination treatment groups (p>0.05). Conclusion The combination of artesunate and T. crispa extract is better in decreasing NFêB and ICAM-1 expression in the brain of mouse malaria models.

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