Prevention And Treatment Of Gastric Mucosal Injury Induced By Antiplatelet Drug With Panax Quinquefolius Saponin

The study consists of two parts:clinical study and experimental one.Study I:Clinical studyObjective:To observe the differences between coronary heart disease (CHD) patients taking dual-antiplatelet drug and CHD patients taking single-antiplatelet drug on gastrointestinal adverse reactions.Methods:A total of949CHD patients were designed into two cohorts. The1st cohort which consisted of348CHD patients took only aspirin or clopidogrel, the other cohort patients which consisted of601CHD patients took both aspirin and clopidogrel.A one-year follow-up was finished by the out-patient meeting and telephone inquiry, endpoint events and gastrointestinal adverse reactions were investigated.Results:There is no significant differences between ingle-antiplatelet group and dual-antiplatelet group in the incidence of nausea or vomiting, pantothenic acid or heartburn over the same period (P>0.05). AT the sixth month of follow-up, compared with the dual-antiplatet group? the number of gastrointestinal adverse reactions and gastrointestinal adverse reactions credits significantly increased (P<0.05). AT the twelfth month of follow-up, compared with the dual-antiplatet group, the number of gastrointestinal adverse reactions and gastrointestinal adverse reactions credits significantly increased too (P<0.01)Conclusion:Long-term use of antiplatelet drugs aspirin and clopidogrel, can cause gastrointestinal adverse reactions and combination of dual antiplatelet drugs can raise the incidence of gastrointestinal tract adverse reactions.Study Ⅱ:Experimental studyObjective:This study is to observe the effect of panax quinquefolius saponin on gastric mucosal lesion induced by dual-antiplatelet drug.Methods:60SD rats, ligate left anterior descending coronary artery as experimental Acute Myocardial Infarction (Acute Myocardial Infarction, AMI) model. The successful operation of rats were randomly and equally divided into AMI model group (distilled water2ml/kg/d by gavage,12rats)、aspirin group (aspirin9mg/kg/d)、 clopidogrel group (clopidogrel6.75mg/kg/d) and dual antiplatelet group (aspirin9mg/kg/d and clopidogrel6.75mg/kg/d by gavage,12rats)、dual antiplatelet and PQS group(dual antiplatelet and PQS162mg/kg/d by gavage,12rats)、The other12rats were regarded as Sham-operated group(Only puncture not ligation of coronary artery, distilled water2ml/kg/d by gavage,12rats) After duplicating the mold2nd days, distinguish to infuse by corresponding the soup feeding28days. Then under4%chloral hydrate anesthesia, Blood plasma were collected by abdominal aortic method, TO measure serum gastrin (GAS), nitric oxide (NO), interleukin (IL)1β (IL-1beta), tumor necrosis factor alpha (TNF alpha) and plasma motilin (MTL), endothelin (ET1) content, and the changes of histology and ultrastructure of gastric mucosa were observed.Results:Gastric mucosa damage index (Guth score) and pathological grading index of Sham-operated group (Whittle score) and AMI group were zero, Compared with the AMI group, the gastric mucosa Guth score and Whittle score of dual antiplatelet group were significantly increased (P<0.01). Compared with the dual antiplatelet group, dual antiplatelet and PQS group gastric mucosa congestion reduced, inflammatory cell infiltration reduced, stomach surface cells were relatively complete. The Guth score and Whittle score were significantly decreased (P<0.01). Compared with the AMI group, dual antiplatelet group rats plasma ET-1, MTL, serum IL-1β, TNF alpha content elevated significantly (P<0.05), Serum NO and GAS content reduced significantly (P<0.05). Compared with dual antiplatelet group, dual antiplatelet and PQS group Serum NO and GAS content decreased significantly (P<0.05), Plasma ET-1, MTL, serum IL-1β, TNF alpha significantly reduced (P<0.05).Conclusion:PQS has a certain effect for repairing gastric mucosa damage induced by dual-antiplatelet. The mechanism may be related to promoting GAS, NO protection factor formation, reducing inflammatory factor IL-1β, TNF alpha secretion, reducing ET-1, MTL damage factor formation.