Molecular signatures of soil-derived dissolved organic matter constrained by mineral weathering.

Dissolved organic matter (DOM) in soils drives biogeochemical cycling and soil functions in different directions depending on its molecular signature. Notably, there is a distinct paucity of information concerning how the molecular signatures of soil DOM vary with different degrees of weathering across wide geographic scales. Herein, we resolved the DOM molecular signatures from 22 diverse Chinese reference soils and linked them with soil organic matter and weathering-related mineralogical properties. The mixed-effects models revealed that the yields of DOM were determined by soil organic carbon content, whereas the molecular signature of DOM was primarily constrained by the weathering-related dimension. The soil weathering index showed a positive effect on the lability and a negative effect on the aromaticity of DOM. Specifically, DOM in highly weathered acidic soils featured more amino sugars, carbohydrates, and aliphatics, as well as less O-rich polyphenols and condensed aromatics, thereby conferring a higher DOM biolability and lower DOM aromaticity. This study highlights the dominance of the weathering-related dimension in constraining the molecular signatures and potential functions of DOM in soils across a wide geographic scale.

Mastoparan M extracted from Vespa magnifica alleviates neuronal death in global cerebral ischemia-reperfusion rat model.

Objectives: Global cerebral ischemia (GCI), a consequence of cardiac arrest (CA), can significantly damage the neurons located in the vulnerable hippocampus CA1 areas. Clinically, neurological injury after CA contributes to death in most patients. Mastoparan-M extracted from Vespa magnifica (Smith) can be used to treat major neurological disorders. Hence, this study aimed to assess the effects of Mastoparan-M on GCI. Materials and Methods: To evaluate the neurotoxicity and neuroprotective effect of Mastoparan-M, the CCK8 and Annexin V-FITC/PI apoptosis assays were first performed in hippocampal HT22 neuronal cells in vitro. Then, Pulsinelli's 4-vascular occlusion model was constructed in rats. After treatment with Mastoparan-M (0.05, 0.1, and 0.2 mg/kg, IP) for 3 or 7 days, behavioral tests, H&E staining or Nissl staining, immunohistochemistry, and ELISA were employed to investigate neuroprotective effects of Mastoparan-M on GCI in rats. Results: In vitro, the growth of HT22 neuronal cells was restrained at concentrations of 30-300 µg/ml (at 24 hr, IC50=105.2 µg/ml; at 48 hr, IC50=46.81 µg/ml), and Mastoparan-M treatment (0.1,1 and 5 µg/ml) restrained apoptosis. In vivo, Mastoparan-M improved neurocognitive function and neuronal loss in the hippocampal CA1 area of rats. In addition, these effects were associated with the prevention of neuroinflammation, oxidative stress, and apoptosis. Conclusion: Mastoparan-M acts as a neuroprotective agent to alleviate neuronal death in rats.