OBJECTIVE: To probe into the effects of reduced glutathione on inflammatory process and vascular endothelial damage mediated by nicotinamide adenine dinucleotide phosphate oxidase（NOX

2

） in patients with ST segment elevation myocardial infarction（STEMI） undergoing primary percutaneous coronary intervention（PPCI）. METHODS: A total of 252 patients with STEMI addmitted into the hospital from Oct. 2019 to Nov. 2021 were extracted to be divided into the reduced glutathione group and the control group via the random number table

with 126 cases in each group. The reduced glutathione group was treated with intravenous drip of reduced glutathione at a dose of 2.4 g/d once a day on the day of PPCI and from the 1 st to 3 rd day after PPCI. The control group was given placebo. The white blood cell and subtype indicators

oxidative stress indicators

inflammation and endothelial dysfunction indicators

and echocardiographic indicators were compared between two groups before and after PPCI. RESULTS: After 5 d of surgery

the neutrophil/lymphocyte ratio

high-sensitivity C-reactive protein（hs-CRP）

soluble NOX

2

derived peptide（sNOX

2

-dp）

tumor necrosis factor-α（TNF-α） and cardiac troponin T levels in the reduced glutathione group were significantly lower than those in the control group

with statistically significant differences（P

<

0.001）. At the 6 th month of follow-up

the left ventricular end diastolic volume

left ventricular end systolic volume and left ventricular remodeling in the reduced glutathione group were significantly lower than those in the control group

and the left ventricular ejection fraction was significantly higher than those in the control group

with statistically significant difference（P

<

0.001）. sNOX

2

-dp was positively correlated with TNF-α（r=0.052

P

<

0.001）

and negatively correlated with hs-CRP（r=-0.623

P=0.005） and nitric oxide（r=-0.316

P

<

0.001）. CONCLUSIONS: Preventive infusion of reduced glutathione in STEMI patients undergoing PPCI can protect important myocardial components and endothelial cells from harmful pro-oxidative and inflammatory environments

and avoid adverse left ventricular remodeling.