No abstract

This study was performed to examine the beneficial potential of steamed soybean wastewater (SSW), which is generated during the manufacture of fermented soybean products and usually discarded as a by-product. The SSW was found to contain considerable amounts of isoflavones and had concentration-dependent radical scavenging capabilities. Moreover, oral administration of SSW effectively prevented colonic damage induced by dextran sulfate sodium (DSS), based on improvement of morphological and histological features, reduction of oxidative stress indicators, suppression of proinflammatory cytokine production, downregulation of inflammatory marker expression in the colonic tissue, and inhibition of the inflammatory activation of macrophages. It suggests that SSW could prevent intestinal inflammation in humans, although its efficacy should be verified through careful study design in humans. These findings have implications for enhancement of the value-added of SSW and for reduction of wastewater treatment costs incurred by the food industry.

Steamed soybean wastewater (SSW) is a commonly produced as a byproduct for manufacturing soybean food such as chonggukjang, doenjang, and natto, and may contain various water‐soluble and biologically beneficial constituents. In this study, we examined the general composition of SSW and additionally the protective effect against colorectal damage caused by dextran sodium sulfate (DSS) in adult male BALB/c mice. The moisture content in the SSW was 90.8±0.42%, crude protein 1.2±0.02%, crude lipid 0.13±0.01%, crude protein 0.85±0.05%, carbohydrate 7.02±0.32%. For animal study, the lyophilized SSW was dissolved in vehicle (consisting of 5% v/v ethanol, 5% v/v tween‐80, and 90% saline) and orally administered at a dose of 1 g/kg body weight on a daily basis for three weeks. Colorectal damage was induced by providing 3.5% (w/v) DSS in drinking water for the last nine days. We found that oral administration of SSW macroscopically and histologically improved DSS‐induced colorectal injury, reduced expressions of inflammatory cytokines and NF‐κB and its downstream proteins in the colorectal tissue, and decreased molecular markers of oxidative DNA damage (assessed by the plasm level of 8‐OHdG) and lipid peroxidation (measured by the MDA level in liver homogenate). These results suggest that dietary SSW can ameliorate colorectal damage by attenuation of inflammatory response.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Phytochemicals that induce nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2) can lower cellular oxidative stress and thus favor cell viability. Considering our previous in vitro study demonstrating that strong antioxidative called luteolin interfered with the anticancer effect of oxaliplatin on HCT116, we hypothesized that luteolin administration would be unadvantageous during oxaliplatin‐based chemotherapy. To test this hypothesis, HCT116 xenograft mouse model was established in BALB/c nude mice. Once palpable tumors were developed after HCT116 cells were subcutaneously transplanted on both flanks of each mouse, mice were randomly allocated into four groups that were intraperitoneally injected with (1) vehicle only (control), (2) oxaliplatin at a dose of 10 mg/kg body weight (BW), (3) luteolin at 50 mg/kg BW, or (4) combination of luteolin and oxaliplatin. Tumor size and body weight were regularly monitored (three times a week) for three weeks. Results demonstrated that oxaliplatin treatment inhibited the growth of xenografted tumors as expected, luteolin treatment had little effect on the tumor size, and combinatorial treatment of oxaliplatin and luteolin most suppressed tumor growth. In addition, oxaliplatin‐luteolin combo reduced heme oxygenase‐1 (HO‐1) protein expression compared to oxaliplatin alone. Moreover, luteolin alone treatment enhanced protein expressions of p53 and its downstream molecule p21. These findings were suggestive of in vivo synergistic effect of combinatorial treatment of oxaliplatin and luteolin at the tested doses in this study and the possible coordinated regulation via p53 and/or HO‐1‐mediated cytoprotection in HCT116 xenograft tumor growth. According to the current observations, our hypothesis ought to be reconsidered; luteolin could advantageously hamper tumor growth during oxaliplatin treatment in colon cancer.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.