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Berrak Yegen - One of the best experts on this subject based on the ideXlab platform.
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halofuginone a specific inhibitor of Collagen Type 1 synthesis ameliorates oxidant colonic damage in rats with experimental colitis
Digestive Diseases and Sciences, 2010Co-Authors: Berna Karakoyun, Emine Salva, Isil Isik, Meral Yuksel, Feriha Ercan, Berrak YegenAbstract:To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 μg/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue Collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue Collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.
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Halofuginone, a Specific Inhibitor of Collagen Type 1 Synthesis, Ameliorates Oxidant Colonic Damage in Rats with Experimental Colitis
Digestive Diseases and Sciences, 2010Co-Authors: Berna Karakoyun, Emine Salva, Isil Isik, Meral Yuksel, Feriha Ercan, Berrak YegenAbstract:To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 μg/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue Collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue Collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.
Berna Karakoyun - One of the best experts on this subject based on the ideXlab platform.
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halofuginone a specific inhibitor of Collagen Type 1 synthesis ameliorates oxidant colonic damage in rats with experimental colitis
Digestive Diseases and Sciences, 2010Co-Authors: Berna Karakoyun, Emine Salva, Isil Isik, Meral Yuksel, Feriha Ercan, Berrak YegenAbstract:To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 μg/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue Collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue Collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.
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Halofuginone, a Specific Inhibitor of Collagen Type 1 Synthesis, Ameliorates Oxidant Colonic Damage in Rats with Experimental Colitis
Digestive Diseases and Sciences, 2010Co-Authors: Berna Karakoyun, Emine Salva, Isil Isik, Meral Yuksel, Feriha Ercan, Berrak YegenAbstract:To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 μg/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue Collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue Collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.
John Scott Roth - One of the best experts on this subject based on the ideXlab platform.
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Hernia Repair Strength Enhanced With Antioxidants.
Journal of Surgical Research, 2020Co-Authors: Vashisht Madabhushi, Job C. Tharappel, Crystal F. Totten, Satya Alluri, John Scott RothAbstract:Abstract Background Incisional hernia is one of the most common complications of abdominal surgery, and repairs are associated with significant recurrence rates. Mesh repairs are associated with the best outcomes, but failures are not uncommon. Doxycycline has been demonstrated to enhance mesh hernia repair outcomes with associated increases in Collagen deposition and improved tensiometric strength. This study compares the outcomes of incisional hernia repair with doxycycline administration and the antioxidant tempol. Materials and methods Twenty-eight male Sprague Dawley rats underwent a midline hernia creation and an intraabdominal polypropylene mesh repair. The animals were administered saline, doxycycline, tempol, or both, daily for 8 wk. The abdominal wall was harvested at 8 wk and tensiometric strength and biochemical analysis was performed. Results The tensiometric strength of the repair was increased in all experimental groups. Collagen Type 1 deposition was increased, and Collagen Type 3 deposition was decreased in each of the experimental groups relative to control. There was no difference in MMP-2 and MMP-9 levels between control and experimental groups. Conclusions The hernia repair strength is equally enhanced with the administration of doxycycline or tempol. Dual therapy provided no benefit over treatment with either single agent. All treatment groups had an increase in Collagen Type 1:3 ratios, but the mechanism is not well understood. The benefits of antioxidant treatment following hernia repair are similar to treatment with doxycycline. Given the high frequency of incisional hernia repair failures, this study has implications for improving outcomes following ventral hernia repair through the use of either doxycycline or antioxidant therapy.
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Doxycycline alters Collagen composition following ventral hernia repair
Surgical Endoscopy, 2017Co-Authors: Job C. Tharappel, Crystal F. Totten, Jennifer W. Harris, Brittany A. Zwischenberger, John Scott RothAbstract:Background Doxycycline, a nonspecific metalloproteinase (MMP) inhibitor, has been demonstrated to impact the strength of the polypropylene (PP) mesh-repaired hernia with an increase in the deposition of Collagen Type 1. The impact of doxycycline with porcine acellular dermal matrices (PADM) is unknown; therefore, we evaluated the impact of doxycycline administration upon hernia repair with PP and PADM mesh. Methods Sprague–Dawley rats weighing ~400 g underwent laparotomy with creation of a midline ventral hernia. After a 27-day recovery, animals were randomly assigned to four groups of eight and underwent intraperitoneal underlay hernia repair with either PP or PADM. Groups were assigned to daily normal saline (S) or daily doxycycline in normal saline 10 mg/kg (D) via oral gavage for 8 weeks beginning 24 h preoperatively. Animals were euthanized at 8 weeks and underwent tensiometric testing of the abdominal wall and western blot analyses for Collagen subTypes and MMPs. Results Thirty-two animals underwent successful hernia creation and repair with either PADM or PP. At 8 weeks, 15 of 16 PP-implanted animals survived with only 12 of 16 PADM-implanted animals surviving. There were no differences in the mesh to fascial interface tensiometric strength between groups. Densitometric counts in the PADM-D group demonstrated increased Collagen Type 1 compared to PP-S (PADM-D [1286.5], PADM-S [906.9], PP-S [700.4], p = 0.037) and decreased Collagen Type 3 compared to PP-S (PADM-D [7446.9], PADM-S [8507.6], PP-S [11,297.1], p = 0.01). MMP-9 levels were increased in PADM-D (PP-S vs. PADM-D, p = 0.04), while MMP-2 levels were similar between PADM-D and PADM-S, respectively. Conclusions Collagen Type 1 deposition at the mesh to fascial interface is enhanced following administration of doxycycline in ventral hernia repairs with porcine acellular dermal matrices. Doxycycline administration may have implications for enhancing hernia repair outcomes using biologic mesh.
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Doxycycline alters Collagen composition following ventral hernia repair
Surgical Endoscopy and Other Interventional Techniques, 2016Co-Authors: Job C. Tharappel, Crystal F. Totten, Jennifer W. Harris, Brittany A. Zwischenberger, John Scott RothAbstract:Doxycycline, a nonspecific metalloproteinase (MMP) inhibitor, has been demonstrated to impact the strength of the polypropylene (PP) mesh-repaired hernia with an increase in the deposition of Collagen Type 1. The impact of doxycycline with porcine acellular dermal matrices (PADM) is unknown; therefore, we evaluated the impact of doxycycline administration upon hernia repair with PP and PADM mesh. Sprague–Dawley rats weighing ~400 g underwent laparotomy with creation of a midline ventral hernia. After a 27-day recovery, animals were randomly assigned to four groups of eight and underwent intraperitoneal underlay hernia repair with either PP or PADM. Groups were assigned to daily normal saline (S) or daily doxycycline in normal saline 10 mg/kg (D) via oral gavage for 8 weeks beginning 24 h preoperatively. Animals were euthanized at 8 weeks and underwent tensiometric testing of the abdominal wall and western blot analyses for Collagen subTypes and MMPs. Thirty-two animals underwent successful hernia creation and repair with either PADM or PP. At 8 weeks, 15 of 16 PP-implanted animals survived with only 12 of 16 PADM-implanted animals surviving. There were no differences in the mesh to fascial interface tensiometric strength between groups. Densitometric counts in the PADM-D group demonstrated increased Collagen Type 1 compared to PP-S (PADM-D [1286.5], PADM-S [906.9], PP-S [700.4], p = 0.037) and decreased Collagen Type 3 compared to PP-S (PADM-D [7446.9], PADM-S [8507.6], PP-S [11,297.1], p = 0.01). MMP-9 levels were increased in PADM-D (PP-S vs. PADM-D, p = 0.04), while MMP-2 levels were similar between PADM-D and PADM-S, respectively. Collagen Type 1 deposition at the mesh to fascial interface is enhanced following administration of doxycycline in ventral hernia repairs with porcine acellular dermal matrices. Doxycycline administration may have implications for enhancing hernia repair outcomes using biologic mesh.
Feriha Ercan - One of the best experts on this subject based on the ideXlab platform.
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halofuginone a specific inhibitor of Collagen Type 1 synthesis ameliorates oxidant colonic damage in rats with experimental colitis
Digestive Diseases and Sciences, 2010Co-Authors: Berna Karakoyun, Emine Salva, Isil Isik, Meral Yuksel, Feriha Ercan, Berrak YegenAbstract:To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 μg/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue Collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue Collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.
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Halofuginone, a Specific Inhibitor of Collagen Type 1 Synthesis, Ameliorates Oxidant Colonic Damage in Rats with Experimental Colitis
Digestive Diseases and Sciences, 2010Co-Authors: Berna Karakoyun, Emine Salva, Isil Isik, Meral Yuksel, Feriha Ercan, Berrak YegenAbstract:To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 μg/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue Collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue Collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.
Meral Yuksel - One of the best experts on this subject based on the ideXlab platform.
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halofuginone a specific inhibitor of Collagen Type 1 synthesis ameliorates oxidant colonic damage in rats with experimental colitis
Digestive Diseases and Sciences, 2010Co-Authors: Berna Karakoyun, Emine Salva, Isil Isik, Meral Yuksel, Feriha Ercan, Berrak YegenAbstract:To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 μg/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue Collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue Collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.
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Halofuginone, a Specific Inhibitor of Collagen Type 1 Synthesis, Ameliorates Oxidant Colonic Damage in Rats with Experimental Colitis
Digestive Diseases and Sciences, 2010Co-Authors: Berna Karakoyun, Emine Salva, Isil Isik, Meral Yuksel, Feriha Ercan, Berrak YegenAbstract:To evaluate the effect of halofuginone on trinitrobenzene sulfonic acid (TNBS)-induced colonic injury, rats were given halofuginone (40 μg/kg, intraperitoneally) or saline 1 h before the induction of colitis, and the injections were continued twice daily for 3 days until they were decapitated. High macroscopic and microscopic damage scores, elevated colonic wet weights, colonic myeloperoxidase activity, malondialdehyde and tissue Collagen level, and luminol chemiluminescence values, and marked reduction in glutathione level of the saline-treated colitis group were all reversed by treatment with halofuginone. In conclusion, halofuginone exerts beneficial effects in TNBS-induced colonic inflammation in rats. The anti-inflammatory effects of halofuginone appear to involve suppression of neutrophil accumulation, preservation of endogenous glutathione, and inhibition of reactive oxidant generation. Halofuginone also shows antifibrotic effect via inhibition of tissue Collagen production. The present data encourage possible use of the antifibrotic halofuginone as an anti-inflammatory agent in improving oxidative injury in colitis.