Protective Effect Of Ammonium Dihydromyricetin On Acute Alcoholic Gastric Mucosal Injury In Mice

AIM: To study the effect of Dihydromyricetin derivative ammonium dihydromyricetin on acute alcoholic gastric mucosal injury in mice?METHODS: 35 C57BL/6J mice(SPF,6-8 weeks old,18-22g)were randomly divided into five experimental groups: normal group,model group,dihydromyricetin group(5mg/kg),ammonium dihydromyricetin group(5ml/kg),ammonium dihydromyricetin group(10ml/kg),7 mice in each group.After a week of adaptive feeding,all mice fasting water for 24 hours,normal group and model group were gaveged normal saline(10 mL/kg),the other three groups were gaveged corresponding drugs(10 mL/kg);after 30 minutes,normal group were gaveged normal saline(12.5 ml/Kg),and the remaining mice were gaveged 56 degrees Red Star Erguotou(12.5 ml/kg).After 6 hours of anesthesia with ether,the mice in each group were executed.The gastric tissues were separated and cut open along the great curvature.The gastric cavity was cleaned with ice saline and spread on the clean plate.The general changes were observed and the injury index and ulcer inhibition rate were calculated.Gastric homogenate was prepared,IL-6,TNF-? and IL-10 were detected by ELISA,SOD by WST-1,MDA by TBA and MPO by colorimetry and analyzed statistically.Results:1 General state of mice: mice in the normal group had the best mental state,normal activity,good movement and climbing;mice in the model group showed symptoms such as unstable gait,decreased activity,inactivity and sleepiness after alcohol administration;mice treated with dihydromyricetin and ammonium dihydromyricetin had milder symptoms than those in the model group,and were less active than those in the normal group.2 General condition of gastric: The structure of gastric in the normal group was intact,and the injury in the model group was the most obvious.Hemorrhage and erosion could be seen in the model group.The degree of hemorrhage and erosion in the drug prevention group was lighter than that in the model group.3 Ulcer index and inhibition rate: Compared with model group(38.33±8.05),low TDHM group(29.83±7.10),high TDHM group(25.16±6.54)and DHM group(26.16±6.14)could significantly reduce gastric tissue injury index(P < 0.05,inhibit ulcer formation;the inhibition rate of ulcer was 22.17%,34.3%,33.05%,respectively);but there was no significant difference in injury index among the three drug groups.4 Changes of IL-6,TNF-? and IL-10 levels in gastric tissue: Compared with the normal group(24.97±9.50ng/g),the level of IL-6 in the model group(42.21±6.16ng/g)was significantly higher(P < 0.01).The level of IL-6 in DHM group and low TDHM group did not decrease significantly(41.03±+7.44ng/g,32.14 ±10.23ng/g,VS model group,P > 0.05,P > 0.05).The level of IL-6 in the high TDHM group decreased significantly(28.79±4.90 ng/g VS model group,P < 0.05).Compared with the normal group(214.03±41.41ng/g),the level of TNF-? in model group(300.09±22.65 ng/g)was significantly higher(P < 0.01),while the level of TNF-? in DHM group was not significantly decreased(270.19±32.99 ng/g VS model group,P > 0.05).Both low TDHM and high TDHM could significantly reduce the level of TNF-?(224.02±17.47/g,224.56±32.12 ng/g VS model group,P < 0.05,P < 0.05).Compared with the normal group(212.25+75.71 ng/g),the level of IL-10 in the model group(212.06±46.75 ng/g)did not change significantly.The level of IL-10 increased after DHM administration,but there was no statistical difference(235.34±21.55 ng/g VS model group,P > 0.05).The level of IL-10 in the low TDHM and high TDHM groups increased significantly(339.35±40.98 ng/g,348.89±80.45 ng/g,VS model group,all P < 0.01).5 Changes of SOD activity in gastric tissue: Compared with normal group(1.92±0.56 U/mgprot),SOD activity in model group(3.61±0.62 U/mgprot)increased,but there was no statistical difference(P > 0.05).SOD activity in DHM group increased after intragastric administration,but there was no statistical difference(4.50±2.71 U/mgprot VS model group,P >0.05).SOD activity increased significantly after intragastric administration of low TDHM and high TDHM(6.73±2.37 U/mgprot,6.71 U/mgprot,60 ± 2.41 U/mgprot,VS model group,P < 0.05,P < 0.05).6 Changes of MDA level in gastric tissues: Compared with normal group(10.28±4.23 nmol/mgprot),MDA level in model group(23.75±5.66 nmol/mgprot)was significantly elevated(P < 0.01),MDA level in DHM group decreased slightly,but no statistical difference(21.66 <6.96 nmol/mgprot,P > 0.05),MDA levels in low TDHM and high TDHM group were significantly decreased(13.07±5.40 nmol/mgprot,10.58±4.60 nmol/mgprot,VS model group,P < 0.05,P < 0.01).7 Changes of MPO activity in gastric tissues: Compared with the normal group(5.86±3.68U/g),the MPO level in model group(14.66±3.73 U/g)increased significantly(P <0.01),and decreased after DHM administration(9.68±4.71 U/g VS model group,P>0.05),and decreased significantly after low TDHM and high TDHM administration(8.12±4.69 U/g,7.01±5.11 U/g VS model group,all P <0.05).Conclusion:1 Ammonium dihydromyricetin can alleviate acute alcohol-induced gastric mucosal injury,which may be related to the alleviation of alcohol-induced gastric inflammation and oxidative stress injury.2 The protective effects of ammonium dihydromyricetin(5mg/kg and 10mg/kg)on acute alcoholic gastric mucosal injury were not significantly different.The anti-inflammatory and anti-oxidative effects of ammonium dihydromyricetin were stronger than dihydromyricetin.