Raloxifene is a nonsteroidal selective estrogen receptor modulator that has favorable effects on markers of cardiovascular risk and has been associated with a reduced risk of coronary heart disease (CHD) in postmenopausal women. Raloxifene also has antiestrogenic effects on the breast and in animals has suppressed the growth of estrogen-stimulated mammary cancers. The Raloxifene Use for The Heart (RUTH) trial was a randomized, double-blind, placebo-controlled study carried out at 177 sites in 26 countries. The 10,101 participants were women aged 55 and older who were at least 12 months postmenopausal and who either had established CHD or were at increased risk. They were assigned to receive either 60 mg raloxifene orally each day or a placebo. The 2 groups were similar in baseline characteristics except for slightly higher cardiovascular risk scores for women assigned to raloxifene. During a median follow up of 5.6 years, no significant differences were found with respect to deaths from coronary causes, nonfatal myocardial infarction, or hospital admission because of an acute coronary syndrome. Women with established CHD and those at increased risk for CHD had similar outcomes. For the primary coronary outcome, the results of as-treated analyses were comparable to those of intention-to-treat analyses. Raloxifene was associated with a decreased incidence of invasive breast cancer; the hazard ratio was 0.56 with a 95% confidence interval of 0.38 to 0.83. The absolute risk reduction for every 1000 women given raloxifene for 1 year was 1.2 cases for both invasive breast cancer and estrogen receptor-positive invasive breast cancer. Among secondary outcomes, the incidence of stroke did not differ significantly between the raloxifene and placebo groups, but fatal strokes were 49% more frequent in raloxifene-treated women. Venous thromboembolic events were 44% more frequent in the raloxifene group. Incidence rates of all breast cancers and of clinical vertebral fractures were lower in the raloxifene group. More than 90% of women in both groups reported adverse events. Rates of discontinuance because of side effects were 22% in the raloxifene group and 20% in the placebo group. Serum levels of low-density lipoprotein cholesterol declined in women given raloxifene but increased in placebo recipients. Levels of high-density lipoprotein cholesterol increased in both groups but more so in women treated with raloxifene. Raloxifene treatment, given for a median of over 5 years to postmenopausal women at increased risk of CHD, did not significantly alter CHD risk in the RUTH study. Its beneficial effects in lowering the risk of invasive breast cancer and vertebral fracture must be weighed against increased risks of fatal stroke and venous thromboembolism.

/pdf/effects-of-raloxifene-on-cardiovascular-events-and-breast-228vetfkn7.pdf

Effects of raloxifene on cardiovascular events and breast cancer in postmenopausal women

Tissue regeneration is a vital phenomenon in the skeletal system of human beings during their life span. The structure of bony architecture and teeth are highly dependent to this ongoing procedure to maintain their functional form. Regarding the fundamental function of our skeletal system, all the involved components are at constant risk for injuries and deformations throughout the life. Therefore, in modern medicine, promotion of bone and tooth regeneration has become a critical counter measure to correct these acquired defects. There are numerous ways to address the bone and tooth related erosive pathologies but utilization of natural compounds has gained immense popularity in recent years. These materials provide a broad spectrum of therapeutic agents with a variety of biological characteristics. In this review, a comprehensive exploration has been implemented to extract and categorize the relevant scientific evidence on this issue, based on the source of natural candidates and the potential clinical indications. Database searching presented a considerable data pool with more than 300 references in this field. According to the results, all the proposed items can be categorized in two major groups including scaffolding and osteogenesis (or dentinogenesis) induction. The clinical applicability of a number of them is properly demonstrated in clinical trials but for the rest, more examinations are required to reach a conclusive decision.

Current natural bioactive materials in bone and tooth regeneration in dentistry: a comprehensive overview

Osteoarthritis (OA), the commonest arthritis, is characterized by the progressive destruction of cartilage, leading to disability. The Current early clinical treatment strategy for OA often centers on anti‐inflammatory or analgesia medication, weight loss, improved muscular function and articular cartilage repair. Although these treatments can relieve symptoms, OA tends to be progressive, and most patients require arthroplasty at the terminal stages of OA. Recent studies have shown a close correlation between joint pain, inflammation, cartilage destruction and synovial cells. Consequently, understanding the potential mechanisms associated with the action of synovial cells in OA could be beneficial for the clinical management of OA. Therefore, this review comprehensively describes the biological functions of synovial cells, the synovium, together with the pathological changes of synovial cells in OA, and the interaction between the cartilage and synovium, which is lacking in the present literature. Additionally, therapeutic approaches based on synovial cells for OA treatment are further discussed from a clinical perspective, highlighting a new direction in the treatment of OA.

The potential role of synovial cells in the progression and treatment of osteoarthritis

Milk contains various bioactive components with osteoanabolic properties. This study investigates the comparative effect of the whey-derived antioxidative (YVEEL) and angiotensin-converting enzyme inhibitory (YLLF) bioactive peptides on bone remodelling in ovariectomised (OVX) osteoporotic rat model. OVX animals were administered with antioxidative (AO) (500 μg kg−1 day−1) and angiotensin-converting enzyme inhibitory (ACE inhibitory) (50 μg kg−1 day−1) peptides for eight weeks. Trabecular microarchitectural parameters of femoral and tibiae bone were determined using micro-CT scan. Bone formation, resorption, turnover markers (ALP, RANKL, OCN) and inflammatory cytokines (TNF-α, TGF-β, IFN-γ) were determined by ELISA. Both AO and ACE inhibitory peptides inhibited the increase in bone turnover and inflammatory cytokines while increased the bone formation markers. The altered morphometric parameters of femoral and tibiae bones due to OVX were strikingly attenuated by the peptide administration. The results indicated that AO peptide exerts more osteoprotective potential than ACE inhibitory peptide by suppressing inflammatory status and enhancing bone formation markers.

Evaluation of the osteoprotective potential of whey derived-antioxidative (YVEEL) and angiotensin-converting enzyme inhibitory (YLLF) bioactive peptides in ovariectomised rats

Western lifestyle contributes to an overt increase in the prevalence of metabolic anomalies including diabetes mellitus (DM) and obesity. Prevalence of DM is rapidly growing worldwide, affecting many individuals in both developing and developed countries. DM is correlated with the onset and development of complications with diabetic nephropathy (DN), diabetic cardiomyopathy (DC) and diabetic neuropathy being the most devastating pathological events. On the other hand, Nrf2 is a regulator for redox balance in cells and accounts for activation of antioxidant enzymes. Dysregulation of Nrf2 signaling has been shown in various human diseases such as DM. This review focuses on the role Nrf2 signaling in major diabetic complications and targeting Nrf2 for treatment of this disease. These three complications share similarities including the presence of oxidative stress, inflammation and fibrosis. Onset and development of fibrosis impairs organ function, while oxidative stress and inflammation can evoke damage to cells. Activation of Nrf2 signaling significantly dampens inflammation and oxidative damage, and is beneficial in retarding interstitial fibrosis in diabetic complications. SIRT1 and AMPK are among the predominant pathways to upregulate Nrf2 expression in the amelioration of DN, DC and diabetic neuropathy. Moreover, certain therapeutic agents such as resveratrol and curcumin, among others, have been employed in promoting Nrf2 expression to upregulate HO-1 and other antioxidant enzymes in the combat of oxidative stress in the face of DM. 

Nrf2 signaling in diabetic nephropathy, cardiomyopathy and neuropathy: Therapeutic targeting, challenges and future prospective

Asperosaponin VI (ASA VI), a natural compound isolated from the well-known traditional Chinese herb Radix Dipsaci, has an important role in promoting osteoblast formation. However, its effects on osteoblasts in the context of osteoporosis is unknown. This study aimed to investigate the effects and mechanism of ASA VI action on the proliferation and osteogenic differentiation of bone marrow stromal cells isolated from the ovariectomized rats (OVX rBMSCs). The toxicity of ASA VI and its effects on the proliferation of OVX rBMSCs were measured using a CCK-8 assay. Various osteogenic differentiation markers were also analyzed, such as ALP activity, calcified nodule formation, and the expression of osteogenic genes, i.e., ALP, OCN, COL 1 and RUNX2. The results indicated that ASA VI promoted the proliferation of OVX rBMSCs and enhanced ALP activity and calcified nodule formation. In addition, while ASA VI enhanced the expression of ALP, OCN, Col 1 and RUNX2, treatment with LY294002 reduced all of these osteogenic effects and reduced the p-AKT levels induced by ASA VI. These results suggest that ASA VI promotes the osteogenic differentiation of OVX rBMSCs by acting on the phosphatidylinositol-3 kinase/AKT signaling pathway.

/pdf/asperosaponin-vi-promotes-bone-marrow-stromal-cell-59wpje6sdd.pdf

Asperosaponin VI promotes bone marrow stromal cell osteogenic differentiation through the PI3K/AKT signaling pathway in an osteoporosis model.

Suboptimal light stress in grapevines is increasing worldwide with the spread of grapevine cultivation, which can affect grapevine physiology and productivity, such as in Southern China. Abscisic acid (ABA) is an important hormone in plant adaptive responses to abiotic stress, including low light stress. However, ABA signaling pathway genes (APGs) are not well characterized in the grapevine, and little is known of their potentially mitigating role in grapevine growth under weak light stress. Our study aimed to explore the potential role of the ABA signaling pathway in the response of grapevines to suboptimal light conditions. In this study, APGs were identified in the grapevine genome, and the distribution of conserved motifs was shown to reflect their phylogenetic relationships. Gene duplication analysis indicated that segmental duplication was an important driver for gene expansion in the grapevine ABA signaling pathway. Suboptimal conditions of light were shown to seriously affect the growth of grapevine leaves and berries, with the differential regulation of APGs in the grapevine. Our study summarizes the basic characteristics of APGs in grapevine, which can now be examined further for their roles in grapevine’s response to suboptimal light conditions.

Identification of ABA Signaling Pathway Genes and Their Differential Regulation in Response to Suboptimal Light Stress in Grape (Vitis vinifera L.)

Cartilage regeneration is dependent on cellular-extracellular matrix (ECM) interactions. Natural ECM plays a role in mechanical and chemical cell signaling and promotes stem cell recruitment, differentiation and tissue regeneration in the absence of biological additives, including growth factors and peptides. To date, traditional tissue engineering methods by using natural and synthetic materials have not been able to replicate the physiological structure (biochemical composition and biomechanical properties) of natural cartilage. Techniques facilitating the repair and/or regeneration of articular cartilage pose a significant challenge for orthopedic surgeons. Whereas, little progress has been made in this field. In recent years, with advances in medicine, biochemistry and materials science, to meet the regenerative requirements of the heterogeneous and layered structure of native articular cartilage (AC) tissue, a series of tissue engineering scaffolds based on ECM materials have been developed. These scaffolds mimic the versatility of the native ECM in function, composition and dynamic properties and some of which are designed to improve cartilage regeneration. This review systematically investigates the following: the characteristics of cartilage ECM, repair mechanisms, decellularization method, source of ECM, and various ECM-based cartilage repair methods. In addition, the future development of ECM-based biomaterials is hypothesized.

Preparation and Application of Decellularized ECM-Based Biological Scaffolds for Articular Cartilage Repair: A Review

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Asperosaponin VI promotes bone marrow stromal cell osteogenic differentiation through the PI3K/AKT signaling pathway in an osteoporosis model.

Identification of ABA Signaling Pathway Genes and Their Differential Regulation in Response to Suboptimal Light Stress in Grape (Vitis vinifera L.)

Preparation and Application of Decellularized ECM-Based Biological Scaffolds for Articular Cartilage Repair: A Review