Because of the high incidence of cardiovascular diseases in Asian countries, traditional fermented foods from Asia have been increasingly investigated for antiatherosclerotic effects. This study investigated the production of nattokinase, a serine fibrinolytic enzyme, in pigeon pea by Bacillus subtilis fermentation. B. subtilis 14714, B. subtilis 14715, B. subtilis 14716, and B. subtilis 14718 were employed to produce nattokinase. The highest nattokinase activity in pigeon pea was obtained using B. subtilis 14715 fermentation for 32 hours. In addition, the levels of antioxidants (phenolics and flavonoids) and angiotensin converting enzyme inhibitory activity were increased in B. subtilis 14715-fermented pigeon pea, compared with those in nonfermented pigeon pea. In an animal model, we found that both water extracts of pigeon pea (100 mg/kg body weight) and water extracts of B. subtilis-fermented pigeon pea (100 mg/kg body weight) significantly improved systolic blood pressure (21 mmHg) and diastolic blood pressure (30 mmHg) in spontaneously hypertensive rats. These results suggest that Bacillus-fermented pigeon pea has benefits for cardiovascular health and can be developed as a new dietary supplement or functional food that prevents hypertension.

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RMDE treatment inhibited the growth of SCC-25 cells by arresting cell cycle at the G2/M phase and induced apoptosis in a time- and dose-dependent manner. Therefore RMDE may be a good candidate for development as a dietary supplement against oral cancer.

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Previous studies have established that red mold rice can regulate blood pressure in spontaneously hypertensive rats (SHR) and that Monascus -fermented products, including monacolin K, ankaflavin (AF), and monascin (MS), can inhibit expression of adhesion factors such as E-selectin and endothelin-1 to prevent human acute monocytic leukemia cell line THP-1 monocytes from adhering to human aortic endothelial cells. However, it remains unknown whether AF and MS act directly on human umbilical endothelial cells (HUVECs) to enhance nitric oxide (NO) synthesis through the stimulation of endothelial NO synthase (eNOS) expression. To address this knowledge gap, this study investigated whether AF and MS directly regulate NO synthesis and attenuate adhesion factor expression induced by treatment with tumor necrosis factor-α (TNF-α) in HUVECs. The results revealed that both AF and MS (20 μM) treatments promoted increases in eNOS expression and decreases in vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and endothelin-1 mRNA and protein expression resulting from 12 h of TNF-α treatment. These effects are attributed to the ability of AF and MS to inhibit extracellular signal-regulated protein kinase (ERK) phosphorylation and nuclear factor κB (NF-κB) translocation from the cytoplasm into the nucleus, thereby exerting antihypertensive activity.

Extracellular vesicle (EV)-mediated intercellular communication acts as a critical culprit in cancer development. The selective packaging of oncogenic molecules renders tumor-derived EVs capable of altering the tumor microenvironment and thereby modulating cancer developments that may contribute to drug resistance and cancer recurrence. Moreover, the molecular and functional characteristics of cancer through its development and posttreatment evolve over time. Tumor-derived EVs are profoundly involved in this process and can, therefore, provide valuable real-time information to reflect dynamic changes occurring within the body. Because they bear unique molecular profiles or signatures, tumor-derived EVs have been highlighted as valuable diagnostic and predictive biomarkers as well as novel therapeutic targets. In addition, the use of an advanced EV-based drug delivery system for cancer therapeutics has recently been emphasized in both basic and clinical studies. In this review, we highlight comprehensive aspects of tumor-derived EVs in oncogenic processes and their potential clinical applications.

These findings indicated that IPE and D-pinitol possess beneficial effects for neural protection and memory ability in a rat model of diabetes.

Abstract:Chemotherapy is the main approach for treating advanced and recurrent carcinoma, but the clinical performance of chemotherapy is limited by relatively low response rates, drug resistance, and adverse effects that severely affect the quality of life of patients. An association between epithelial-mesenchymal transition (EMT) and chemotherapy resistance has been investigated in recent studies. Our recent studies have found that the aqueous extract of Solanum nigrum (AESN) is a crucial ingredient in some traditional Chinese medicine formulas for treating various types of cancer patients and exhibits antitumor effects. We evaluated the suppression of EMT in MCF-7 breast cancer cells treated with AESN. The mitochondrial morphology was investigated using Mitotracker Deep-Red FM stain. Our results indicated that AESN markedly inhibited cell viability of MCF-7 breast cancer cells through apoptosis induction and cell cycle arrest mediated by activation of caspase-3 and production of reactive oxygen species. Furthermore, mitochondrial fission was observed in MCF-7 breast cancer cells treated with AESN. In addition to elevation of E-cadherin, downregulations of ZEB1, N-cadherin, and vimentin were found in AESN-treated MCF-7 breast cancer cells. These results suggested that AESN could inhibit EMT of MCF-7 breast cancer cells mediated by attenuation of mitochondrial function. AESN could be potentially beneficial in treating breast cancer cells, and may be of interest for future studies in developing integrative cancer therapy against proliferation, metastasis, and migration of breast cancer cells.