Autophagy is a ‘self-eating’ system that regulates the degradation of cellular components and is involved in various biological processes including survival and development. However, despite its crucial role in organisms, the regulatory mechanism of autophagy remains largely unclear, particularly in invertebrates. In this study, conserved autophagy in the rotifer Brachionus koreanus in response to cadmium (Cd) exposure was verified by measuring acidic vesicle organelles using acridine orange (AO) and neutral red (NR) staining, and by detecting LC3 I/II on Western blot and immunofluorescence. We also demonstrated activation of p38 mitogen-activated protein kinase (MAPK) in response to Cd-induced oxidative stress, leading to the induction of autophagy in B. koreanus. This was further verified by analysis of MAPK protein levels and immunofluorescence of LC3 I/II after treatment with reactive oxygen species (ROS) scavengers and inhibitors specific to MAPKs. We propose a p38 MAPK-mediated regulatory mechanism of autophagy in B. koreanus in response to Cd-induced oxidative stress. This study will contribute to a better understanding of autophagic processes in invertebrates and its modulation by environmental stressors.

自噬是一种“自食”系统，可调节细胞成分的降解，并参与各种生物过程，包括生存和发育。然而，尽管自噬在生物​​中起着至关重要的作用，但自噬的调控机制仍不清楚，尤其是在无脊椎动物中。在这项研究中，通过使用Bra啶橙（AO）和中性红（NR）染色测量酸性囊泡细胞器，并通过Western blot检测LC3 I / II，验证了轮虫Brachionus koreanus对镉（Cd）暴露的保守自噬。和免疫荧光。我们还证明了p38丝裂原活化蛋白激酶（MAPK）的激活响应Cd诱导的氧化应激，从而导致了朝鲜小芽孢杆菌自噬的诱导。。通过用活性氧（ROS）清除剂和MAPK特异性抑制剂处理后，MAPK蛋白水平和LC3 I / II的免疫荧光分析进一步证实了这一点。我们提出了p38 MAPK介导的朝鲜芽孢杆菌自噬对Cd诱导的氧化应激反应的调控机制。这项研究将有助于更好地了解无脊椎动物的自噬过程及其受环境应激因素的调节。