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The beneficial effects of melatonin on abiotic stress have been demonstrated in several plants. However, little is known about the signal transduction pathway of melatonin involved in the plant stress response. Here, we manipulated the melatonin levels in tomato plants through a chemical approach. The roles of melatonin in stress tolerance were studied by assessing the symptoms, chlorophyll fluorescence and stress-responsive gene expression. Moreover, both chemical and genetic approaches were used to study the roles of hydrogen peroxide (H O ) in melatonin-induced signal transduction in tomato plants. We found that melatonin activates NADPH oxidase (RBOH) to enhance H O levels by reducing its S-nitrosylation activity. Furthermore, melatonin-induced H O accumulation was accompanied by obtainable stress tolerance. Inhibition of RBOH or chemical scavenging of H O significantly reduced the melatonin-induced defense response, including reduced expression of several stress-related genes (CDPK1, MAPK1, TSPMS, ERF4, HSP80 and ERD15) and reduced antioxidative enzyme activity (SOD, CAT and APX), which were responsible for the stress tolerance. Collectively, these results revealed a novel mechanism in which RBOH activity and H O signaling are important components of the melatonin-induced stress tolerance in tomato plants.

SPMC, with better tolerability and less frequent adverse events, demonstrated non-inferior bowel cleaning efficacy than that of the PEG. Large-scale, well-organized, head-to-head studies are warranted.

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Electroacupuncture (EA) has been used worldwide to treat demyelinating diseases, but its therapeutic mechanism is poorly understood. In this study, a custom-designed model of compressed spinal cord injury (CSCI) was used to induce demyelination. Zusanli (ST36) and Taixi (KI3) acupoints of adult rats were stimulated by EA to demonstrate its protective effect. At 14 days after EA, both locomotor skills and ultrastructural features of myelin sheath were significantly improved. Phenotypes of proliferating cells were identified by double immunolabeling of 5-ethynyl-2'-deoxyuridine with antibodies to cell markers: NG2 [oligodendrocyte precursor cell (OPC) marker], 2',3'-cyclic-nucleotide 3'-phosphodiesterase (CNPase) (oligodendrocyte marker), and glial fibrillary acidic protein (GFAP) (astrocyte marker). EA enhanced the proliferation of OPCs and CNPase, as well as the differentiation of OPCs by promoting Olig2 (the basic helix-loop-helix protein) and attenuating Id2 (the inhibitor of DNA binding 2). EA could also improve myelin basic protein (MBP) and protect existing oligodendrocytes from apoptosis by inhibiting caspase-12 (a representative of endoplasmic reticulum stress) and cytochrome c (an apoptotic factor and hallmark of mitochondria). Therefore, our results indicate that the protective effect of EA on neural myelin sheaths is mediated via promotion of oligodendrocyte proliferation and inhibition of oligodendrocyte death after CSCI.

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