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Nitric oxide (NO)-releasing aspirin and (NO) donors in protection of gastric mucosa against stress.
J Physiol Pharmacol. 2008 Aug; 59 Suppl 2:103-15.JP

Abstract

Acute gastric mucosal lesions represent an important clinical problem. The experimental model of acute gastritis such as water immersion restraint (WRS) stress is useful tool in examination of pathomechanism of acute gastric damage. Nitric oxide (NO) plays an important role in the maintenance of gastric barrier, however the role of reactive oxygen species (ROS) in the interaction between NO and gastric mucosa integrity has been little studied. The purpose of our present study was to explain the participation of ROS in healing of WRS-induced gastric lesions accelerated by NO. Experiments were carrying out on 120 male Wistar rats. To assess gastric blood flow (GBF) laser Doppler flowmeter was used. The number of gastric lesions was established by planimetry. The colorimetric assays were used to determine gastric tissue level of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), the products of lipid peroxidation by ROS, as well as superoxide dismutase (SOD) activity, the enzyme scavanger of ROS. We demonstrated that 3.5 h of WRS resulted in appearance of acute gastric mucosal lesions accompanied by a significant decrease of GBF. Biological effects of ROS were estimated by measuring tissue level of MDA and 4-HNE, as well as the SOD activity. It was demonstrated that 3.5 h of WRS led to significant increase of MDA and 4-HNE mucosal level, that was accompanied by a decrease of SOD activity. Pretreatment with NO-donors (SIN-1, SNAP, nitroglycerin, NO-ASA) resulted in reduction of gastric lesions number, increment of GBF, decrease of MDA and 4-HNE tissue level and increase of SOD activity. Suppression of ROS play an important role in NO-donors action in gastroprotection against gastric acute lesions induced by 3.5 h of WRS. NO-donors cause an attenuation of lipid peroxidation as documented by a decrease of MDA and 4-HNE levels and enhancement of antioxidative properties as evidenced by increase of SOD activity.

Authors+Show Affiliations

Department of Physiology Jagiellonian University Medical College, Cracow, Poland.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18812632

Citation

S Kwiecien, S, et al. "Nitric Oxide (NO)-releasing Aspirin and (NO) Donors in Protection of Gastric Mucosa Against Stress." Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, vol. 59 Suppl 2, 2008, pp. 103-15.
S Kwiecien S, Pawlik MW, Brzozowski T, et al. Nitric oxide (NO)-releasing aspirin and (NO) donors in protection of gastric mucosa against stress. J Physiol Pharmacol. 2008;59 Suppl 2:103-15.
S Kwiecien, S., Pawlik, M. W., Brzozowski, T., Konturek, P. C., Sliwowski, Z., Pawlik, W. W., & Konturek, S. J. (2008). Nitric oxide (NO)-releasing aspirin and (NO) donors in protection of gastric mucosa against stress. Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, 59 Suppl 2, 103-15.
S Kwiecien S, et al. Nitric Oxide (NO)-releasing Aspirin and (NO) Donors in Protection of Gastric Mucosa Against Stress. J Physiol Pharmacol. 2008;59 Suppl 2:103-15. PubMed PMID: 18812632.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitric oxide (NO)-releasing aspirin and (NO) donors in protection of gastric mucosa against stress. AU - S Kwiecien,S, AU - Pawlik,M W, AU - Brzozowski,T, AU - Konturek,P C, AU - Sliwowski,Z, AU - Pawlik,W W, AU - Konturek,S J, PY - 2008/06/10/received PY - 2008/07/25/accepted PY - 2008/10/1/pubmed PY - 2008/12/17/medline PY - 2008/10/1/entrez SP - 103 EP - 15 JF - Journal of physiology and pharmacology : an official journal of the Polish Physiological Society JO - J Physiol Pharmacol VL - 59 Suppl 2 N2 - Acute gastric mucosal lesions represent an important clinical problem. The experimental model of acute gastritis such as water immersion restraint (WRS) stress is useful tool in examination of pathomechanism of acute gastric damage. Nitric oxide (NO) plays an important role in the maintenance of gastric barrier, however the role of reactive oxygen species (ROS) in the interaction between NO and gastric mucosa integrity has been little studied. The purpose of our present study was to explain the participation of ROS in healing of WRS-induced gastric lesions accelerated by NO. Experiments were carrying out on 120 male Wistar rats. To assess gastric blood flow (GBF) laser Doppler flowmeter was used. The number of gastric lesions was established by planimetry. The colorimetric assays were used to determine gastric tissue level of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), the products of lipid peroxidation by ROS, as well as superoxide dismutase (SOD) activity, the enzyme scavanger of ROS. We demonstrated that 3.5 h of WRS resulted in appearance of acute gastric mucosal lesions accompanied by a significant decrease of GBF. Biological effects of ROS were estimated by measuring tissue level of MDA and 4-HNE, as well as the SOD activity. It was demonstrated that 3.5 h of WRS led to significant increase of MDA and 4-HNE mucosal level, that was accompanied by a decrease of SOD activity. Pretreatment with NO-donors (SIN-1, SNAP, nitroglycerin, NO-ASA) resulted in reduction of gastric lesions number, increment of GBF, decrease of MDA and 4-HNE tissue level and increase of SOD activity. Suppression of ROS play an important role in NO-donors action in gastroprotection against gastric acute lesions induced by 3.5 h of WRS. NO-donors cause an attenuation of lipid peroxidation as documented by a decrease of MDA and 4-HNE levels and enhancement of antioxidative properties as evidenced by increase of SOD activity. SN - 1899-1505 UR - https://www.unboundmedicine.com/medline/citation/18812632/Nitric_oxide__NO__releasing_aspirin_and__NO__donors_in_protection_of_gastric_mucosa_against_stress_ L2 - https://www.lens.org/lens/search/patent/list?q=citation_id:18812632 DB - PRIME DP - Unbound Medicine ER -