Evidence-based complementary and alternative medicine : eCAM · 2022
Pretreatment with Shenmai Injection Protects against Coronary Microvascular Dysfunction.
СтатьяНазвание и аннотация: Перевод в очереди
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Zheng Zhaohai, Yu Zhangjie, Xu Buyun, Zhou Yan, Xing Yangbo, Li Qingsong, Tang Weiliang, Peng Fang
Аннотация
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.
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.