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Background. The clinical treatment of coronary microvascular dysfunction (CMD) is mainly based on conventional medicine, but the mechanism of the medicine is single and the efficacy is different. Shenmai injection (SMI) has a variety of ingredients, but the effect of SMI on CMD has not been studied. This study investigated the effect of SMI on CMD and its possible mechanism. Methods. The protective effect of SMI on CMD was evaluated in Sprague-Dawley (SD) rats and human umbilical vein endothelial cells (HUVECs). In vivo, forty-five male SD rats were randomly divided into control group (sham group), CMD group (model group), and SMI group (treatment group). Two weeks after SMI intervention, laurate was injected into the left ventricle of rats to construct a CMD model. Blood samples were collected to detect myocardial enzymes, oxidative stress, and inflammatory factors, and the hearts of rats were extracted for histopathological staining and western blot detection. In vitro, a hydrogen peroxide-induced endothelial injury model was established in HUVECs. After pretreatment with SMI, cell viability, oxidative stress, vasodilative factors, and apoptosis were detected. Results. In vivo, pretreatment with SMI could effectively reduce the concentrations of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), endothelin-1 (ET-1), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and malondialdehyde (MDA) in the serum of rats. Meanwhile, the expression of bcl-2-associated X (Bax) and caspase-3 protein in the myocardium of rats was decreased in the SMI group. The levels of nitric oxide (NO) and superoxide dismutase (SOD) and the expression of B-cell lymphoma-2 (Bcl-2) were higher in the SMI group than in the CMD group. Pathological staining results showed that SMI could effectively reduce inflammatory infiltration and the formation of collagen fibers and microthrombus in the rat myocardium. In vitro, intervention with SMI could improve endothelial function in a dose-dependent manner as evidenced by increasing the activity of endothelial cells and the expression of NO, SOD, endothelial nitric oxide synthase (eNOS), and Bcl-2, while decreasing cell apoptosis and the levels of ET-1, MDA, Bax, and caspase-3. Conclusions. Pretreatment with SMI could improve CMD by alleviating oxidative stress, inflammatory response, and apoptosis and then improving vascular endothelial function and microvascular structure.

Objective. This study aimed to investigate the effect of Xuefu Zhuyu decoction on preventing contrast-induced nephropathy (CIN) after percutaneous coronary intervention (PCI). Methods. A total of 256 patients undergoing selective PCI for coronary artery disease were consecutively enrolled and randomly divided into two groups: Group A (n = 126) and Group B (n = 130). Before and after PCI, all patients routinely received antiplatelet aggregation therapy, antilipidemic therapy, and hydration therapy. Besides routine therapy, patients in Group B received Xuefu Zhuyu decoction from 3 days before PCI to 3 days after PCI. Serum creatinine (Scr), estimated glomerular filtration rate (eGFR), superoxide dismutase (SOD), and malondialdehyde (MDA) were measured, respectively, at baseline (72 h before PCI) and at 24, 48, and 72 h after PCI. Results. Compared with Group A, Group B presented a lower fluctuation of SCr and eGFR (P<0.01). The incidence of CIN was less in Group B. According to the definition, CIN occurred in 5 patients (2.0%) in the intervention group and 5 (4.0%) in the control group (P=0.167). In terms of oxidative stress, Group B had a lower MDA (P<0.05), but a higher SOD (P<0.05). Conclusions. Compared with the control group, Xuefu Zhuyu decoction intervention therapy increased the level of SOD and reduced MDA. The Xuefu Zhuyu decoction intervention group presented a higher level of eGFR at 24, 48, and 72 h after PCI in patients with coronary heart disease and a lower level of Scr. The results are propitious to prove that Xuefu Zhuyu decoction might play an antioxidative stress role in the prevention of CIN after PCI.