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Soil salinization negatively affects rice growth and yield; however, how different sludge sources regulate rice growth and yield under salt stress was rarely investigated. This study evaluated the performance of two salt-tolerant rice cultivars, Chaoyou 1000 and Longliangyou 506, grown in two sediment sources, pond sediment (PS) and river sludge (RS), under salt stress (56 ds m−1 brine irrigation) with conventional soil (CS) used as the control. The results showed that the rice yield under the PS and RS treatments was enhanced by 51.0% and 43.6% as compared with CS, respectively, owing to an improvement in spikelet per panicle, 1000-grain weight, dry matter accumulation, and the chlorophyll content in both rice cultivars. Compared with CS, the total nitrogen accumulation, nitrogen grain production efficiency, nitrogen harvest index, and nitrogen partial productivity under the PS and RS treatments were increased by 18.9–28.9%, 17.0–20.6%, 7.2–16.6%, and 43.8–50.9%, respectively. Moreover, rice grown in PS and RS showed higher activities of nitrogen metabolism-related enzymes (nitrate reductase, glutamine synthetase, and glutamate synthetase) at the heading stage and higher K+ and K+/Na+ contents in the leaves. Overall, a balanced utilization of sediment resources (especially pond sediment) can effectively alleviate salt stress and improve the yield and nitrogen use efficiency in rice. [ABSTRACT FROM AUTHOR]

Osteoporosis is an age-related systemic bone disease that places a heavy burden on patients and society. In this study, we aimed to investigate the effects of naringin (NAR) on the osteogenic differentiation of human adipose-derived stromal cells (ADSCs). The results demonstrated that NAR pretreatment effectively abated H2O2-induced cell death and ROS accumulation in ADSCs undergoing osteogenic differentiation (ADSCs-OD). In addition, we also observed that the impaired extracellular matrix mineralization and ALP activity in H2O2-stimulated ADSCs-OD were notably rescued by NAR pretreatment. Moreover, the effects of H2O2 exposure on Wnt/β-catenin signaling in ADSCs-OD were largely reversed by NAR pretreatment. Collectively, our findings indicated that NAR could protect ADSCs-OD against H2O2-inhibited osteogenic differentiation. [ABSTRACT FROM AUTHOR]

Osteoporosis is an age-related systemic bone disease that places a heavy burden on patients and society. In this study, we aimed to investigate the effects of naringin (NAR) on the osteogenic differentiation of human adipose-derived stromal cells (ADSCs). The results demonstrated that NAR pretreatment effectively abated H 2 O 2 -induced cell death and ROS accumulation in ADSCs undergoing osteogenic differentiation (ADSCs-OD). In addition, we also observed that the impaired extracellular matrix mineralization and ALP activity in H 2 O 2 -stimulated ADSCs-OD were notably rescued by NAR pretreatment. Moreover, the effects of H 2 O 2 exposure on Wnt/ β -catenin signaling in ADSCs-OD were largely reversed by NAR pretreatment. Collectively, our findings indicated that NAR could protect ADSCs-OD against H 2 O 2 -inhibited osteogenic differentiation., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2022 Xufang Yang et al.)

Renal ischemia-reperfusion injury (IRI) is the main cause of acute kidney injury (AKI). Many studies on renal IRI have been performed recently, but effective treatments are still lacking. Evidence exists that small endogenous noncoding RNAs are involved in the ischemia-reperfusion process. This article aims to investigate whether microRNA-205 (miR-205) is involved in this process and to determine its role in the hypoxia-induced injury of renal tubular epithelial cells (TECs). We found that miR-205 was significantly downregulated in rats with renal IRI and in HK-2 cells with hypoxia-reoxygenation injury (HRI) in vitro. In vitro, overexpression of intracellular miR-205 by transfection of a miR-205 mimic significantly reduced apoptosis, and this antiapoptotic effect was antagonized by a miR-205 inhibitor. Moreover, we confirmed that PTEN is a target of miR-205. miR-205 exerted its protective effect by inhibiting HK-2 cell apoptosis and promoting HK-2 cell proliferation by inhibiting the expression of PTEN during HRI, and this protective effect was blocked by silencing PTEN. Therefore, we confirmed that miR-205 may target the PTEN/Akt signaling pathway to alleviate hypoxia-induced renal cell damage. miR-205 may be a new potential target for the treatment of renal IRI., Competing Interests: None., (AJTR Copyright © 2019.)