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Drug: Indomethacin

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Total 19 results found since Jan 2013.

Sinomenine increases adenosine A < sub > 2A < /sub > receptor and inhibits NF- κB to inhibit arthritis in adjuvant-induced-arthritis rats and fibroblast-like synoviocytes through α7nAChR
J Leukoc Biol. 2021 Aug 23. doi: 10.1002/JLB.3MA0121-024RRRR. Online ahead of print.ABSTRACTSinomenine (SIN) is a clinical drug for treating rheumatoid arthritis (RA) in China. Our previous study found SIN inhibited inflammation via alpha7 nicotinic acetylcholine receptor (α7nAChR) in macrophages in vitro. Adenosine receptor A2A has anti-inflammatory and immunosuppressive function. However, the mechanisms of SIN acting on α7nAChR and the effect on adenosine A2A receptor (A2A R) in RA are not clear. In the present study, the effects of SIN on adjuvant-induced-arthritis (AIA) rats in vivo and on fibroblast-like synoviocyte...
Source: Journal of Leukocyte Biology - August 23, 2021 Category: Hematology Authors: Lang Yi Junyu Ke Jiayan Liu Huili Lai Yanjun Lv Chong Peng Yingkun Zhi Qun Du Liang Liu Peixun Wang Hua Zhou Yan Dong Source Type: research

Mitigated NSAID-induced apoptotic and autophagic cell death with Smad7 overexpression.
In this study, we explored the role of Smad7 on NSAID-induced cytotoxicity in gastric epithelial cells. Using RGM1 cells, we have compared biological changes between mock-transfected and Smad7-overexpressed cells. As results, significantly decreased cytotoxicity accompanied with decreased levels of cleaved caspase-3 and poly (ADP-ribose) polymerase, Bax, and autophagic vesicles concurrent with decreased expressions of autophagy protein 5 and microtubule-associated protein light chain 3B-II were noted in Smad7-overexpressed cells with indomethacin administration compared to mock-transfected cells. Contrast to mitigated apop...
Source: Journal of Clinical Biochemistry and Nutrition - February 8, 2017 Category: Nutrition Tags: J Clin Biochem Nutr Source Type: research

Therapeutic mechanisms of ibuprofen, prednisone and betamethasone in osteoarthritis.
In conclusion, prednisone, ibuprofen and betamethasone may prevent OA by suppressing the expression of IL‑6 and IL‑8, subsequently inactivating NF‑κB and STAT3 pathways, and ultimately, leading to decreased levels of collagen I, MMP‑1, and MMP‑13. PMID: 28035387 [PubMed - as supplied by publisher]
Source: Molecular Medicine Reports - January 1, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Resveratrol Treatment Inhibits Proliferation of and Induces Apoptosis in Human Colon Cancer Cells.
CONCLUSIONS These findings suggest that resveratrol treatment can be a promising strategy for the treatment of colon cancer. PMID: 27040803 [PubMed - in process]
Source: Medical Science Monitor - April 5, 2016 Category: Research Tags: Med Sci Monit Source Type: research

Indomethacin-Induced Intestinal Epithelial Cell Damage is Mediated by pVHL Activation through the Degradation of Collagen I and HIF-1α.
Abstract Non-steroidal anti-inflammatory drug (NSAID)-induced epithelial cell damage occurs not only in the stomach but also in the intestines and colon. Although several studies have investigated the related mechanism underlying lower gastrointestinal tract injury, the details of this mechanism are still unclear. Since it was reported that protein degradation might play an important role, herein, we focused on one of the major ubiquitin E3 ligases, the von Hippel-Lindau protein (pVHL). To understand whether pVHL is involved in the observed cell damage, we examined whether indomethacin (IM) treatment affects pVHL ...
Source: Biochemical and Biophysical Research communications - November 6, 2015 Category: Biochemistry Authors: Yokoe S, Nakagawa T, Kojima Y, Higuchi K, Asahi M Tags: Biochem Biophys Res Commun Source Type: research

Inhibition of Kv Channel Expression by NSAIDs Depolarizes Membrane Potential and Inhibits Cell Migration by Disrupting Calpain Signaling.
Abstract Clinical use of non-steroidal anti-inflammatory drugs (NSAIDs) is well known to cause gastrointestinal ulcer formation via several mechanisms that include inhibiting epithelial cell migration and mucosal restitution. The drug-affected signaling pathways that contribute to inhibition of migration by NSAIDs are poorly understood, though previous studies have shown that NSAIDs depolarize membrane potential and suppress expression of calpain proteases and voltage-gated potassium (Kv) channel subunits. Kv channels play significant roles in cell migration and are targets of NSAID activity in white blood cells, ...
Source: Biochemical Pharmacology - November 5, 2015 Category: Drugs & Pharmacology Authors: Silver K, Littlejohn A, Thomas L, Marsh E, Lillich JD Tags: Biochem Pharmacol Source Type: research

Apoptosis induction by combination of drugs or a conjugated molecule associating non-steroidal anti-inflammatory and nitric oxide donor effects in medullary thyroid cancer models: implication of the tumor suppressor p73
Conclusion Association of NO with NSAID exhibited amplified anti-tumoral effects on in vitro and in vivo MTC models by inducing p73-dependent apoptotic cell death.
Source: Thyroid Research - August 14, 2015 Category: Endocrinology Source Type: research

Endogenous prostaglandin E2 potentiates anti-inflammatory phenotype of macrophage through the CREB-C/EBPβ cascade.
This article is protected by copyright. All rights reserved. PMID: 26118414 [PubMed - as supplied by publisher]
Source: European Journal of Immunology - June 27, 2015 Category: Allergy & Immunology Authors: Na YR, Jung D, Yoon B, Lee WW, Seok SH Tags: Eur J Immunol Source Type: research

Endogenous prostaglandin E2 potentiates anti‐inflammatory phenotype of macrophage through the CREB‐C/EBPβ cascade
This article is protected by copyright. All rights reserved
Source: European Journal of Immunology - June 1, 2015 Category: Allergy & Immunology Authors: Yi Rang Na, Daun Jung, Boreum Yoon, Won Woo Lee, Seung Hyeok Seok Tags: Regular Article Source Type: research

Eugenol dilates mesenteric arteries and reduces systemic BP by activating endothelial cell TRPV4 channels
Conclusions and ImplicationsEugenol activates TRPV4 channels in mesenteric artery endothelial cells, leading to vasorelaxation, and reduces systemic BP in vivo. Eugenol may be therapeutically useful as an antihypertensive agent and is a viable molecular candidate from which to develop second‐generation TRPV4 channel activators that reduce BP.
Source: British Journal of Pharmacology - May 19, 2015 Category: Drugs & Pharmacology Authors: Dieniffer Peixoto‐Neves, Qian Wang, Jose H Leal‐Cardoso, Luciana V Rossoni, Jonathan H Jaggar Tags: RESEARCH PAPER Source Type: research

Major involvement of Na+‐dependent multivitamin transporter (SLC5A6/SMVT) in uptake of biotin and pantothenic acid by human brain capillary endothelial cells
This study is the first to confirm expression of SLC5A6 in human brain microvessels and to provide evidence that SLC5A6 is a major contributor to luminal uptake of biotin and pantothenic acid at the human BBB. This article is protected by copyright. All rights reserved.
Source: Journal of Neurochemistry - March 21, 2015 Category: Neurology Authors: Yasuo Uchida, Katsuaki Ito, Sumio Ohtsuki, Yoshiyuki Kubo, Takashi Suzuki, Tetsuya Terasaki Tags: Original Article Source Type: research

The molecular mechanism underlying the induction of hepatic MRP3 expression and function by omeprazole
This study aimed to assess changes in fold‐induction of MRP3 mRNA and protein expression over controls in omeprazole‐treated HepG2 cells after transient transfection of human MRP3 siRNA, or after pretreatment of actinomycin D (Act‐D). Furthermore, MRP3 siRNA knock‐down or MRP‐specific inhibition (indomethacin) was used to determine whether induced MRP3 protein by omeprazole could possess enhanced efflux transport. The results demonstrated that omeprazole induced MRP3 mRNA and protein expression in a concentration‐ and time‐dependent manner. Moreover, that induction was almost completely abolished by addition ...
Source: Biopharmaceutics and Drug Disposition - December 1, 2014 Category: Drugs & Pharmacology Authors: Yu‐Qin Pan, Qiong‐Yu Mi, Bang‐Shun He, Shu‐Li Zhao, Ting Tai, Hong‐Guang Xie Tags: Original Paper Source Type: research

Sc-36 * reciprocal interaction of pge2 and wnt signaling regulates cancer stem cells in glioblastoma
The concept of oncogene addiction presupposes that cancer cells require certain dominant oncogenic signals for growth and survival. A profound implication of this hypothesis is that antagonizing this crucial pathway should have significant effects on cancer cells, while sparing normal cells that are not similarly addicted. Clinically, the recognition of oncogenes to which a cancer is addicted could have profound resonance for targeted cancer therapy. The Wnt signaling pathway has recently been described to be constitutively activated in a subgroup of glioblastomas. Here, we performed a systematic review of high-throughput ...
Source: Neuro-Oncology - November 3, 2014 Category: Cancer & Oncology Authors: Wu, M., Nusrat, L., Celebre, A., Bredel, M., Karamchandani, J., Morshead, C., Das, S. Tags: STEM CELLS Source Type: research

Autocrine prostaglandin E2 signaling promotes promonocytic leukemia cell survival via COX-2 expression and MAPK pathway.
Abstract The COX-2/PGE2 pathway has been implicated in cancer occurrence and progression. The underlying mechanisms that facilitate production of COX-2 and its mediator PGE2 in cancer survival remain unknown. Herein, we investigated both PGE2-inducible COX-2 expression and signaling in HL-60 cells following menadione treatment. PGE2 activated anti-apoptotic proteins such as Bcl-2 and Bcl-xL and reduced pro-apoptotic proteins, thereby enhancing cell survival. PGE2 not only induced COX-2 expression but also prevented casapse-3, PARP, and lamin B cleavage. Silencing and inhibition of COX-2 with siRNA transfection or ...
Source: BMB Reports - June 26, 2014 Category: Biochemistry Authors: Shehzad A, Lee J, Lee YS Tags: BMB Rep Source Type: research