Revegetation pattern affecting accumulation of organic carbon and total nitrogen in reclaimed mine soils.

Selecting optimal revegetation patterns, i.e., patterns that are more effective for soil organic carbon (SOC) and total nitrogen (TN) accumulation, is particularly important for mine land reclamation. However, there have been few evaluations of the effects of different revegetation patterns on the SOC and TN in reclaimed mine soils on the Loess Plateau, China. In this study, the SOC and TN stocks were investigated at reclaimed mine sites (RMSs), including artificially revegetated sites (ARSs) (arbors (Ar), bushes (Bu), arbor-bush mixtures (AB), and grasslands (Gr)) and a natural recovery site (NRS), as well as at undisturbed native sites (UNSs). Overall, the SOC and TN stocks in the RMSs were lower than those in the UNSs over 10-13 years after reclamation. The SOC stocks in the RMSs and UNSs only differed in the top 0-20 cm of the soil (p < 0.05). Except for those in Ar, the SOC and TN stocks in the ARSs were significantly larger than those in the NRS (p < 0.05). Compared with those in the NRS, the total SOC stocks in the 100 cm soil interval increased by 51.4%, 59.9%, and 109.9% for Bu, AB, and Gr, respectively, and the TN stocks increased by 33.1%, 35.1%, and 57.9%. The SOC stocks in the 0-100 cm soil interval decreased in the order of Gr (3.78 kg m-2) > AB (2.88 kg m-2) ≥ Bu (2.72 kg m-2), and the TN stocks exhibited a similar trend. These results suggest that grasslands were more favorable than woodlands for SOC and TN accumulation in this arid area. Thus, in terms of the accumulation of SOC and TN, grassland planting is recommended as a revegetation pattern for areas with reclaimed mine soils.

MiR-330-3p suppresses phosphoglycerate mutase family member 5 -inducted mitophagy to alleviate hepatic ischemia-reperfusion injury.

Mitochondrial dysfunction plays a central role in hepatic ischemia-reperfusion injury (IRI). The significance of mitophagy in hepatic IRI remains poorly understood. The mechanisms that cause IRI are complex, and many factors are involved in the injury formation process. The miR-330-3p mediates cell proliferation, cell death, and metabolism in various organisms. In this study, the levels of miR-330-3p were significantly downregulated in hepatic IRI, and the number of autophagosomes was increased in response to IRI as obtained under both in vivo and in vitro conditions. These results demonstrate that a reduction in miR-330-3p expression represents an important factor involved with promoting hepatic IRI. Moreover, we found that miR-330-3p interacted with phosphoglycerate mutase family member 5 (PGAM5) to regulate mitophagy. In specific, an overexpression of miR-330-3p diminished PGAM5 levels, which promoted mitophagy in response to IRI. In contrast, a downregulation of miR-330-3p was associated with increased PGAM5 levels leading to increased mitophagy. In conclusion, miR-330-3p suppresses PGAM5-induced mitophagy to alleviate hepatic IRI. Such findings not only reveal some of the mechanistic basis for this microRNA in liver injury, but also provide a foundation for new therapeutic approaches in the treatment of this condition.