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It is well known that crop monoculture can induce negative effects on soil ecosystems and crop productivity. However, little is known about how vegetable monoculture affects the soil nematode community structure and its relationship with vegetable yields. In this study, the composition, abundance, metabolic footprint, and ecological indices of soil nematodes are investigated in monocultures of pumpkin and melon. The relationships between nematode community structure and yields of pumpkin and melon were analyzed by linear regression. Both monoculture soils of pumpkin and melon suppressed the relative abundance of bacterivores but increased the relative abundance of plant parasites. Pumpkin monoculture soils decreased soil nematode diversity but increased the maturity index of plant parasites. Monoculture soils of pumpkin and melon decreased the metabolic footprint of lower- and higher-level trophic groups of the soil food web, respectively. Pumpkin and melon monoculture soils increased the food web indices channel index (CI) but decreased the enrichment index (EI) and the structure index (SI). The monoculture soils of pumpkin and melon led to a more fungal-dominated decomposition pathway and degraded soil food web conditions. The abundance of bacterivores and food web indices EI and SI were positively correlated with soil nutrients and pH, while the abundance of plant parasites and CI were negatively correlated with soil nutrients and pH. Paratylenchus was negatively correlated with pumpkin and melon yields and could be the potential plant parasites threatening pumpkin and melon productions. Redundancy analysis showed that monocultures of pumpkin and melon altered the soil nematode community via soil properties; total N, total P, alkeline-N, and pH were the main driving factors.

Background/Aims: The induction of excessive autophagy by increased levels of oxidative stress is one of the main mechanisms underlying unilateral ureteral obstruction (UUO)-induced vascular endothelial cell dysfunction. Hydrogen sulfide (H2S) has been shown to have an anti-oxidative effect, but its mode of action on excessive autophagy in vascular endothelial cells is unclear. Methods: Surgery was used to induce UUO in male C57BL/6 mice as an in vivo model. Human renal epithelial cells (HK-2) were treated with H2O2 as an in vitro model. NaHS was used as an exogenous H2S donor. Transmission electron microscopy was applied to observe the structure of renal autophagosomes. The expression of proteins related to autophagy and apoptosis was detected by western blot analysis in vivo and in vitro. Flow cytometry (DCFH-DA) was used to examine the levels of intracellular reactive oxygen species (ROS). The terminal deoxynucleotidyl transferase dUTP nick end labeling assay was used to detect cell apoptosis. Compound C was used to analyze the association of AMPK with autophagy. Results: Compared with the sham group, in which the ureter was exposed but not ligated, the cell apoptosis index, number of autophagosomes, protein expression of microtubule-associated protein 1 light-chain 3 (LC3)-II/I, beclin-1, and p-AMPK/AMPK were significantly increased in the UUO group. On the other hand, p62, cystathionine β-synthase, and cystathionine γ-lyase protein expression levels and H2S concentration were significantly decreased (p < 0.05). These alterations were ameliorated by the addition of NaHS (p < 0.05). Similar results were observed in vitro. By using the AMPK inhibitor compound C, it was indicated that AMPK was involved in ROS-induced autophagy. In addition, using tissue from patients with obstructive nephropathy, excessive autophagy was observed by an increased LC3-II/LC3-I ratio. Conclusion: NaHS-treatment may exert a protective effect on mouse kidney against UUO by suppressing the ROS-AMPK pathway. ROS-AMPK-mediated autophagy may represent a promising therapeutic target for obstructive nephropathy.