+GZ Exposure Is Aggravating Gastric Mucosal Injury In Rats Of Oxygen Free Radical Mechanism And Prevention Research

Positive acceleration (+G z) is the head-to-toe generated when theflight direction of acceleration, when the acceleration is greater than sevenis the high positive acceleration.+G z exposure is an importantcontinuing environmental factor in spaceflight activities and the fighterflight, the pilot changed due to the size or direction of the velocity occursduring flight caused by changes in the state of motion, that causes theacceleration motion.The current study shows+G z can cause acute andchronic gastric mucosal lesions, and studies have shown that gastricmucosa damage is closely related to the oxygen free radicals.The mainsubject of study is to explore the changes of gastric mucosal injury in ratswhen expose to+G z and to explore the changes of oxygen free radicalsmetabolism in malondialdehyde (MDA), superoxide dismutase (SOD) andglutathione peroxidase (GSH-Px) in rats and try to give glutathione (GSH)prophylaxis treatment to provide a theoretical basis for the prevention andtreatment of gastrointestinal disease in clinical pilots.A total of60male SD rats were randomly divided into six groups ofcontrol group, ethanol control group,+5Gz value exposure,+10Gz valueexposure, GSH+5Gz value-treated and GSH+10Gz value-treated group(n=10each). Both GSH groups received adaptive feeding for7days andthen intraperitoneal injection of GSH for3consecutive days. After sixgroups fasted24hours within10days and gastric lavage of anhydrousethanol for1hour, control group had no acceleration,+5Gz valueexposure and GSH+5Gz exposure group at+5Gz and the latter groups respectively at+10Gz for around3min. Each group underwent anesthesiaof pentobarbital after centrifuge immediately and stomachs were collectedfor observation of mucosal injury. Mucosal damage index was calculatedby the GUTH methods. The content of mucosa MDA, SOD and activity ofGSH-Px was detected by ELISA.(1) General observation: the normal control group gastric was smoothand complete; ethanol group was relatively smooth and no significantbleeding, and erosion;+5Gz exposure group valued with scatteredbleeding points and small ulcers;+10Gz exposure group valued surfacediffuse edema, erosion widely varying sizes and hemorrhage; GSH+5Gzvalue-treated group had scattered bleeding points and small ulcers; GSH+10Gz value-treated group had gastric surface without significant edema,only have a small amount of bleeding streak stoves.(2) Light microscope:+10Gz exposure group gastric value was heavier structural damaged thanother groups and histological lesions invaded the submucosa and muscular,caused serious tissue damage; GSH pretreatment significantly reducedgastric mucosal injury.(3) Gross lesion index: In addition to the normalcontrol group, the rats had gastric mucosal injury. Ethanol control groupwas10.000(9.225~13.875);+5Gz exposure group values25.400(14.025~30.000); the gastric mucosal damage value of+10Gz exposuregroup was heaviest.It was higher than the first three groups [47.150(41.500~60.050), both P <0.05]. GSH pretreatment can reduce the degreeof mucosa injury, GSH+5Gz value-treated group was13.000(11.025~15.575), and compared with+5Gz exposure group the differencewas statistically significant (P <0.05); GSH+10Gz value value-treatedgroup was9.500(7.500~14.125), representing a statistical difference,compared with+10Gz exposure group (P <0.05).(4) Gastric MDA content:The level of MDA of+5Gz value exposure was no significant differencescompared with the ethanol control group[(0.255±0.074vs0.235±0.044)nmol/mg, P>0.05];+10Gz value exposure was significantly higher than the first three groups(0.377±0.079nmol/mg, P <0.05); GSH protectiongroup was significantly lower than the level of+5Gz and+10Gz valueexposure group (GSH+5Gz:0.185±0.010, GSH+10Gz:0.199±0.021nmol/mg, all P <0.05);(5) Gastric SOD content: The content of SOD of+5Gz value exposure was less than that in the ethanol control group(9.707±0.691vs10.757±0.878U/mg, P <0.05), and the content of+10Gzexposure group mucosa SOD was significantly lower than the first threegroup (8.852±1.001U/mg, all P <0.05); GSH protection group werehigher than the level of+5Gz and+10Gz value exposure group (GSH+5Gz:10.807±1.023, GSH+10Gz:10.365±0.915U/mg, all P <0.05);(6)Gastric GSH-Px activity: The level of GSH-Px of+5Gz value exposurewas higher than the ethanol control group (67.412±5.994vs66.831±9.808U/mg, P <0.05);+10Gz value exposure was significantly lower than thefirst three groups (54.061±5.830U/mg, all P <0.05); GSH+5Gzvalue-treated group was no significantly difference with+5Gz valuegroup(66.899±3.869U/mg, P>0.05); GSH+10Gz value-treated group wasdifferent with+10Gz value and GSH+5Gz value-treated group and therewas a statistical difference (61.509±6.992U/mg, P <0.05).Summary(1)+Gz exposure can increase the acute gastric mucosal injury, and the moresevere+Gz values, the greater injury is;(2) The changes of the gastricmucosa level of MDA, SOD content and GSH-Px activity indicate thatoxygen free radicals play an important role in gastric mucosal injury under+Gz exposure;(3) GSH can reduce the damage extent of the gastricmucosa, maintaining the integrity of the gastric mucosa and when exposedto high+Gz value the gastric mucosal protective effect is more obvious.