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Objective We aimed to (i) investigate the protective effect of active components of water extract of huangqi (milkvetch root) on high glucose (25 mmol/L) induced injury of human umbilical vein endothelial cells (HUVEC) and (ii) elucidate the underlying mechanism. Methods Male SD rats were continuously fed with water extract [20 g/(kg·d)] for 7 d, and blood samples were colleeted 1, 2 and 4 h after the last gavage, combined with supernatant, and performed ultra-performance liquid chromatography (UPLC-MS) analysis to screen the active components of the extract in rats. Cells were divided into normal group, model group, different active components groups treated with different concentrations, and the concerted application of active components group. Cell viability was measured by Cell Counting Kit-8 to explore the optimal concentration of the effective components of milkvetch root. Oxidative damage was measured by reactive oxygen species (ROS). The enzyme-linked immunosorbent assay measured the contents of superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA); the protein expression level of nuclear factor E2 related factor (Nrf 2) and heme oxygenase 1 (HO-1) by Western blotting. Results Formononetin, daidzein, and calycosin are the active components of milkvetch root water extract.Compared with the normal group, the cell viability of the model group was increased (P<0.05). Compared with the model group, cell viability was decreased in each concentration(26, 13, 6.5 μmol/L) of formononetin group (P<0.05), a high dose of daidzein (0.11 μmol/L) could reduce cell viability (P<0.05). Compared with the normal group, the ROS levels in the model group were increased(P<0.05); compared with the model group, the ROS levels in the formononetin high and medium concentrations(26, 13 μmol/L) groups, different concentrations of daidzein (0.11, 0.06, 0.03 μmol/L), the calycosin high concentration group (7.00 μmol/L) were decreased (P<0.05). The combined active components inhibitive rate was higher than the single active components, and highest in the high concentration group. Compared with the normal group, Nrf2 and HO-1 protein expressions were decreased in the model group (P<0.05); compared with the model group, Nrf2 and HO-1 proteins were increased in the group with high concentration of concerted application group (P<0.05). Compared with the normal group, SOD, CAT were decreased (P<0.05), MDA increased (P<0.05) in the model group; compared with the model group, SOD, CAT in the high concentration concerted application group were increased (P<0.05), MDA was significantly decreased (P<0.05). Conclusion The active components of milkvetch root water extract, formononetin, daidzein, calycosin can protect HUVEC from high glucose-induced injury. The mechanism may be related to the regulation of Nrf2, HO-1, SOD, CAT, and MDA expression and their antioxidant effects. [ABSTRACT FROM AUTHOR]

Diabetic cardiomyopathy (DCM) is one of the main complications of diabetic patients and the major reason for the high prevalence of heart failure in diabetic patients. Fufang Xueshuantong (FXST) is a traditional Chinese medicine formula commonly used in the treatment of diabetic retinopathy and stable angina pectoris. However, the role of FXST in DCM has not yet been clarified. This study was conducted to investigate the effects of FXST on diabetic myocardial lesions and reveal its molecular mechanism. The rats were intraperitoneally injected with 65 mg/kg streptozotocin (STZ) to induce diabetes mellitus (DM). DM rats were given saline or FXST. The rats in the control group were intraperitoneally injected with an equal amount of sodium citrate buffer and gavaged with saline. After 12 weeks, echocardiography, heart weight index (HWI), and myocardial pathological changes were determined. The expression of transforming growth factor-beta1 (TGF- β 1), collagen I, and collagen III was examined using immunofluorescence staining and western blot. The expressions of Wnt/ β -catenin signaling pathway-related proteins and mRNA were detected by western blot and real-time PCR. The results showed that FXST significantly improved cardiac function, ameliorated histopathological changes, and decreased HWI in the DM rats. FXST significantly inhibited the expression of myocardial TGF- β 1, collagen I, and collagen III in DM rats. Furthermore, FXST significantly inhibited the Wnt/ β -catenin pathway. Taken together, FXST has a protective effect on DCM, which might be mediated by suppressing the Wnt/ β -catenin pathway., Competing Interests: The authors declare that there are no conflicts of interest., (Copyright © 2022 Meizhong Peng et al.)

Huoxin Pill (HXP), a traditional Chinese medicine, has been prescribed widely in the treatment of coronary heart disease, angina pectoris, and other diseases. However, the possible protective mechanisms of HXP on myocardial ischemia remain unclear. In the current study, we investigated the effects and potential mechanism of HXP on myocardial ischemia and cardiac inflammation and the activation of TLR4/NF- κ B pathway. Determination of electrocardiogram, echocardiography, and heart weight index (HWI) indicated that HXP treatment obviously attenuated the elevation of ST-segment, end-diastolic volume, and HWI in the AMI rat model. Enzyme-linked immunosorbent assay (ELISA) demonstrated that Huoxin Pill treatment significantly decreased the levels of CTnT, CK-MB, MDA, IL-6, and TNF- α , while it increased SOD content in serum of the AMI rat model. Moreover, hematoxylin and eosin (HE) and immunohistochemistry (IHC) staining revealed that HXP treatment alleviated pathological change, infiltration of inflammatory cells, levels of IL-6 and TNF- α , and expression of TLR4 and p-NF- κ B in cardiac tissues of the AMI rat model. In conclusion, HXP treatment significantly improves cardiac function and attenuates cardiac inflammation by suppressing the activation of TLR4/NF- κ B pathway in the ISO-induced AMI rat model. This study provides insights into the potential of HXP on prevention and treatment of AMI., Competing Interests: The authors declare that there are no conflicts of interest regarding the publication of this paper., (Copyright © 2020 Jianfeng Chu et al.)