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BACKGROUND Osteoporosis has become an important public health issue with the increase of aging population, and afflicts millions of people worldwide, particularly elderly or postmenopausal women. In the present study, we prepared compound amino acid chelated calcium (CAA‐Ca) from processing by‐products of Chlamys farreri, and evaluated its effect on postmenopausal osteoporosis with an ovariectomized (OVX) rat model. RESULTS: A 60‐day treatment of OVX rats with CAA‐Ca significantly enhanced the bone mineral density (BMD) and the bone calcium content. Meanwhile, some bone morphometric parameters, trabecular bone number (Tb.N), trabecular bone volume fraction (BV/TV), trabecular bone thickness (Tb.Th) and cortical bone wall thickness (Ct.Th), were also increased by 8.20%, 118.18%, 32.99% and 19.10%, respectively. In addition, the alkaline phosphatase (ALP) levels in serum were significantly reduced after CAA‐Ca treatment, while the blood calcium levels were increased. Mechanistically, CAA‐Ca down‐regulated the levels of receptor activator of nuclear factor‐κB (RANK) and receptor activator of nuclear factor‐κB ligand (RANKL), and up‐regulated osteoprotegerin (OPG) levels in osteoclasts, inhibiting bone resorption and bone loss. Meanwhile, CAA‐Ca treatment raised β‐catenin levels and lowered Dickkopf1 (DKK1) levels in the Wnt signaling pathway of osteoblasts, which can promote calcium absorption and bone formation. CONCLUSION: The results suggested that CAA‐Ca promoted bone formation, inhibited bone resorption and improved bone microstructure. Therefore, this study contributes to the potential application of CAA‐Ca as a functional food resource in the treatment of postmenopausal osteoporosis. © 2021 Society of Chemical Industry [ABSTRACT FROM AUTHOR]

[Display omitted] • Oral administration of RBPs reduced blood pressures in SHRs. • RBPs improved the injuries of kidney, blood vessel and heart in SHRs. • RBPs improved hypertension by inhibiting RAS signaling pathway excessive activation. • RBPs improved hypertension by maintaining ET-1 / NO secretion balance. • RBPs improved intestinal flora disorder in SHRs. In our previous study, the clams (Ruditapes philippinarum) were inoculated with Bacillus natto and fermented to produce peptides (RBPs) with high ACE inhibitory effect in vitro. In this study, we continued to explore the anti-hypertensive effect and potential mechanisms of RBPs in vivo. The results showed that RBPs significantly reduced both systolic and diastolic blood pressure and alleviated the damage of kidney, thoracic aorta and heart of spontaneously hypertensive rats after 8 weeks of treatment. Meanwhile, RBPs could also inhibit the expression of RAS signaling pathway, maintained the secretion balance of NO/ET-1 in vascular endothelial cells and inhibited the cardiac TGF-β/Smad pathway. Most notably, RBPs could also improve the gut microbiota by decreasing the ratio of Firmicutes and Bacteroidetes and increasing the relative abundance of certain genera, like Ruminococcaceae_UCG-014. The data suggested that RBPs could be used as functional food ingredient for the improvement of hypertension. [ABSTRACT FROM AUTHOR]

Epimedium brevicornu Maxim, Dioscorea nipponica Makino , and Salvia miltiorrhiza Bunge formula (EDS) are three traditional Chinese medicines commonly combined and used to treat osteoarthritis (OA). However, the mechanism of its therapeutic effect on OA is still unclear. The aim of this study was to investigate the potential anti osteoarthritis mechanism of EDS in the treatment of OA rats' model by quantitative proteomics. A papain-induced rat OA model was established, and then EDS was intragastrically administered for 28 days. A label-free quantification proteomics was performed to evaluate the holistic efficacy of EDS against OA and identify the possible protein profiles mechanisms. The expression levels of critical changed proteins were validated by RT-qPCR and Western blotting. The effects of EDS were then assessed by evaluating pathologic changes in the affected knee joint and measuring pressure pain threshold, acoustic reflex threshold, angle of joint curvature. Proteomics analysis showed that 62 proteins were significantly upregulated and 208 proteins were downregulated in OA group compared to control group. The changed proteins were involved in activation of humoral immunity response, complement cascade activation, leukocyte mediated immunity, acute inflammatory response, endocytosis regulation, and proteolysis regulation. The EDS treatment partially restored the protein profile changes. The protective effects of EDS on pathologic changes in OA rats' knee joint and pain threshold assessment were consisted with the proteomics results. The results suggest that EDS exerted synergistic therapeutic efficacies to against OA through suppressing inflammation, modulating the immune system, relieving joint pain, and attenuating cartilage degradation. Image 1 [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) and fatigue are two common diseases endangering human life and health that may interact and reinforce one another. Myocardial infarction survivors frequently experience fatigue, and acute myocardial infarction (AMI) is one of the most common cardiovascular diseases that cause fatigue-induced sudden death. Sheng Mai Yin (SMY), a Chinese medicine prescription, is traditionally used for the treatment of diabetes and cardiovascular disease, and has been demonstrated to reduce fatigue and safeguard cardiac function. This study aims to investigate the effects and underlying mechanisms of SMY in treating fatigue and AMI. The pharmacological mechanisms of SMY in treating fatigue and AMI were predicted by bioinformatics and network pharmacology methods. After administering SMY at high, medium and low doses, the swimming time to exhaustion, hemoglobin level, serological parameters and hypoxia tolerance time were detected in C57BL/6N mice, and the left ventricular ejection fractions (LVEF), left ventricular fractional shortening (LVFS), grasp strength, cardiac histopathology, serological parameters and the expression of PINK1 and Parkin proteins were examined in Wistar rats. 371 core targets for SMY and 282 disease targets for fatigue and AMI were obtained using bioinformatics and network pharmacology methods. Enrichment analysis of target genes revealed that SMY might interfere with fatigue and AMI through biological processes such as mitochondrial autophagy, apoptosis, and oxidative stress. For in vivo experiments, SMY showed significant anti-fatigue and hypoxia tolerance effects in mice; It also improved the cardiac function and grasp strength, decreased their cardiac index, myocardial injury and fibrosis degree, and induced serological parameters levels and the expression of PTEN-induced putative kinase 1 (PINK1) and Parkin proteins in myocardium, suggesting that SMY may exert cardioprotective effects in a joint rat model of fatigue and AMI by inhibiting excessive mitochondrial autophagy. This study revealed the anti-fatigue, anti-hypoxia and cardioprotective effects of SMY in a joint model of fatigue-AMI, and the pharmacological mechanism may be related to the inhibition of mitochondrial autophagy in cardiomyocytes through the PINK1/Parkin pathway. The discoveries may provide new ideas for the mechanism study of traditional Chinese medicine, especially complex prescriptions, in treating fatigue and AMI. [Display omitted] • Fatigue and acute myocardial infarction may be related to apoptotic process. • Sheng Mai Yin reduced fatigue, hypoxia and heart damage in mice and rats. • Sheng Mai Yin may suppress PINK1 and Parkin expression in the mitochondrial autophagy of myocardium. [ABSTRACT FROM AUTHOR]