scholarly journals Investigation of cardiovascular protective effect of Shenmai injection by network pharmacology and pharmacological evaluation

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Lin Li ◽  
Dongli Yang ◽  
Jinghao Li ◽  
Lu Niu ◽  
Ye Chen ◽  
...  
Keyword(s):  
Protective Effect ◽  
Network Pharmacology ◽  
Shenmai Injection ◽  
Pharmacological Evaluation

scholarly journals Understanding the Multitarget Pharmacological Mechanism of the Traditional Mongolian Common Herb Pair GuangZao-RouDouKou Acting on Coronary Heart Disease Based on a Bioinformatics Approach

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Jingkun Lu ◽  
Yuchong Hu ◽  
Lechun Wang ◽  
Yuewu Wang ◽  
Shengsang Na ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Myocardial Ischemia ◽  
Protective Effect ◽  
Mechanism Of Action ◽  
Stress Responses ◽  
Inflammatory Responses ◽  
Network Pharmacology ◽  
Therapeutic Effects ◽  
Traditional Mongolian Medicine

GuangZao and RouDouKou (Fructus Choerospondiatis and Nutmeg, FCN) are one of the most common herb pairs in traditional Mongolian medicine for the treatment of coronary heart disease (CHD). However, evidence for the protective effect of FCN is limited, and its underlying mechanism of action remains unclear. The present study employed a network pharmacology approach to identify the potentially active ingredients and synergistic effects of the herb pair FCN as traditional Mongolian medicine. We predicted the targets of all available FCN ingredients with PharmMapper, SWISS, and SuperPred Server and clustered CHD-related targets from the DrugBank and the OMIM database. We also evaluated the links between herbal ingredients and pharmacological actions to explore the potential mechanism of action of FCN. We found that FCN targets a network of CHD-related key processes, including stress responses, cell adhesion and connections, angiogenesis, cell apoptosis and necrosis, the endocrine system, inflammatory and immune responses, and other biological processes. To confirm the predicted results, we investigated the protective effect of FCN on isoproterenol- (ISO-) induced myocardial ischemia in rats. Pathological assessment indicated that FCN inhibits apoptosis and inflammatory responses involving the myocardium. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting analyses demonstrated the therapeutic effects of FCN on ISO-induced myocardial ischemia rats, possibly via regulating stress and inflammatory responses and inhibiting cardiomyocyte apoptosis. The findings of the present study indicate that bioinformatics combined with experimental verification provide a credible and objective method to elucidate the complex multitarget mechanism of action of FCN.

scholarly journals Protective effect of Shenmai injection on doxorubicin-induced cardiotoxicity via regulation of inflammatory mediators

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Sheng Zhang ◽  
Zhen-Qiang You ◽  
Lin Yang ◽  
Li-Li Li ◽  
You-Ping Wu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Inflammatory Mediators ◽  
Inflammatory Cytokine ◽  
Malignant Tumors ◽  
Cardiac Injury ◽  
Viral Myocarditis ◽  
Heart Tissue ◽  
Shenmai Injection ◽  
Cytokine Detection

Abstract Background Doxorubicin (DOX) is a chemotherapy drug for malignant tumors. The clinical application of DOX is limited due to its dosage relative cardiotoxicity. Oxidative damage and cardiac inflammation appear to be involved in DOX-related cardiotoxicity. Shenmai injection (SMI), which mainly consists of Panax ginsengC.A.Mey.and Ophiopogon japonicus (Thunb.) Ker Gawl, is widely used for the treatment of atherosclerotic coronary heart disease and viral myocarditis in China. In this study, we investigated the protective effect of Shenmai injection on doxorubicin-induced acute cardiac injury via the regulation of inflammatory mediators. Methods Male ICR mice were randomly divided into seven groups: control, DOX (10 mg/kg), SMI (5 g/kg), DOX with pretreatment with SMI (0.5 g/kg, 1.5 g/kg or 5 g/kg) and DOX with post-treatment with SMI (5 g/kg). Forty-eight hours after the last DOX administration, all mice were anesthetized for ultrasound echocardiography. Then, serum was collected for biochemical and inflammatory cytokine detection, and heart tissue was collected for histological and Western blot detection. Results A cumulative dose of DOX (10 mg/kg) induced acute cardiotoxicity in mice manifested by altered echocardiographic outcome, and increased tumor necrosis factor, interleukin 6 (IL-6), monocyte chemotactic protein 1, interferon-γ, and serum AST and LDH levels, as well as cardiac cytoplasmic vacuolation and myofibrillar disarrangement. DOX also caused the increase in the expression of IKK-α and iNOS and produced a large amount of NO, resulting in the accumulation of nitrotyrosine in the heart tissue. Pretreatment with SMI elicited a dose-dependent cardioprotective effect in DOX-dosed mice as evidenced by the normalization of serum inflammatory mediators, as well as improve dcardiac function and myofibril disarrangement. Conclusions SMI could recover inflammatory cytokine levels and suppress the expression of IKK-α and iNOS in vivo, which was increased by DOX. Overall, there was evidence that SMI could ameliorate DOX-induced cardiotoxicity by inhibiting inflammation and recovering heart dysfunction.

scholarly journals Shen-Hong-Tong-Luo Formula Attenuates Macrophage Inflammation and Lipid Accumulation through the Activation of the PPAR-γ/LXR-α/ABCA1 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-19
Author(s):  
Zepeng Zhang ◽  
Lu Zhai ◽  
Jing Lu ◽  
Sanmiao Sun ◽  
Dandan Wang ◽  
...  
Keyword(s):  
Protective Effect ◽  
Lipid Accumulation ◽  
High Performance ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Peritoneal Macrophages ◽  
Inflammatory Factors ◽  
Network Pharmacology ◽  
Ppar Γ ◽  
Primary Mouse

Atherosclerosis (AS) is the killer of human health and longevity, which is majorly caused by oxidized lipoproteins that attack macrophages in the endarterium. The Shen-Hong-Tong-Luo (SHTL) formula has shown great clinical efficacy and vascular protective effect for over 30 years in China, to attenuate AS progression. However, its pharmacological mechanism needs more investigation. In this study, we first investigated the chemical composition of SHTL by fingerprint analysis using high-performance liquid chromatography. In primary mouse peritoneal macrophages induced by lipopolysaccharide (LPS), we found that SHTL pretreatment suppressed reactive oxygen species accumulation and reversed the increases of the inflammatory factors, TNF-α and IL-6. Moreover, lipid accumulation induced by oxidized low-density lipoprotein (Ox-LDL) in macrophages was inhibited by SHTL. Additionally, network pharmacology was used to predict the potential targets of SHTL as the PPAR-γ/LXR-α/ABCA1 signaling pathway, which was validated in macrophages and ApoE-/- mice by histopathological staining, qPCR, and Western blot analysis. Importantly, the protective effect of SHTL in the LPS- and Ox-LDL-induced macrophages against inflammation and lipid accumulation was attenuated by GW9662, a PPAR-γ antagonist, which confirmed the prediction results of network pharmacology. In summary, these results indicated that SHTL pretreatment reduced inflammation and lipid accumulation of macrophages by activating the PPAR-γ/LXR-α/ABCA1 pathway, which may provide a new insight into the mechanism of SHTL in the suppression of AS progression.

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