Low­frequency pulsed electromagnetic field promotes functional recovery, reduces inflammation and oxidative stress, and enhances HSP70 expression following spinal cord injury.

Low­frequency pulsed electromagnetic fields (LPEMFs) have been reported to be protective for multiple diseases. However, whether the administration of LPEMFs inhibits inflammation and oxidative stress following spinal cord injury requires further investigation. In the current study, a contusion spinal cord injury model was used and LPEMFs administration was applied to investigate the molecular changes, including inflammation, oxidative stress and heat shock protein 70 (HSP70) levels. The results revealed that LPEMFs significantly promoted functional recovery following spinal cord injury, as demonstrated by an increased Basso, Beattie and Bresnahan score. The results demonstrated that LPEMFs decreased the expression of inflammatory factors, including tumor necrosis factor­α, interleukin­1ß and nuclear factor­κB. Additionally, LPEMFs exposure reduced the levels of inducible nitric oxide synthase and reactive oxygen species, and upregulated the expression of catalase and superoxide dismutase. Furthermore, treatment with LPEMFs significantly enhanced the expression of HSP70 in spinal cord­injured rats. Overall, the present study revealed that LPEMFs promote functional recovery following spinal cord injury, potentially by modulating inflammation, oxidative stress and HSP70.

Full toxicity assessment of Genkwa Flos and the underlying mechanism in nematode Caenorhabditis elegans.

Genkwa Flos (GF), the dried flower bud from Daphne genkwa Sieb. et Zucc. (Thymelaeaceae), is a well-known and widely used traditional Chinese medicine. However, we know little about the in vivo mechanism of GF toxicity. Nematode Caenorhabditis elegans has been considered as a useful toxicity assay system by offering a system best suited for asking the in vivo questions. In the present study, we employed the prolonged exposure assay system of C. elegans to perform the full in vivo toxicity assessment of raw-processed GF. Our data show that GF exposure could induce the toxicity on lifespan, development, reproduction, and locomotion behavior. GF exposure not only decreased body length but also induced the formation of abnormal vulva. The decrease in brood size in GF exposed nematodes appeared mainly at day-1 during the development of adult nematodes. The decrease of locomotion behavior in GF exposed nematodes might be due to the damage on development of D-type GABAergic motor neurons. Moreover, we observed the induction of intestinal reactive oxygen species (ROS) production and alteration of expression patterns of genes required for development of apical domain, microvilli, and apical junction of intestine in GF exposed nematodes, implying the possible dysfunction of the primary targeted organ. In addition, GF exposure induced increase in defecation cycle length and deficits in development of AVL and DVB neurons controlling the defecation behavior. Therefore, our study implies the usefulness of C. elegans assay system for toxicity assessment from a certain Chinese medicine or plant extract. The observed toxicity of GF might be the combinational effects of oxidative stress, dysfunction of intestine, and altered defecation behavior in nematodes.

Transmissions of serotonin, dopamine, and glutamate are required for the formation of neurotoxicity from Al2O3-NPs in nematode Caenorhabditis elegans.

In this study, we investigated genetic mechanisms of neurotransmitters in regulating the formation of adverse effects on locomotion behavior in Al2O3 nanoparticles (NPs)-exposed Caenorhabditis elegans. Al2O3-NPs exposure caused the decrease of locomotion behavior with head thrash and body bend as endpoints. Interestingly, the neurotransmitters of glutamate, serotonin, and dopamine were required for the adverse effects of Al2O3-NPs on locomotion behavior in nematodes. Glutamate transporter EAT-4, serotonin transporter MOD-5, and dopamine transporter DAT-1 might serve as the molecular targets of Al2O3-NPs for neurotoxicity formation. Moreover, the behavioral response of nematodes to Al2O3-NPs exposure was primarily mediated by non-NMDA glutamate receptors GLR-2 and GLR-6, ionotropic serotonin receptor MOD-1, and D1-like dopamine receptor DOP-1. Therefore, Al2O3-NPs exposure influences locomotion behavior of nematodes primarily by impinging on their glutamatergic, serotoninergic, and dopaminergic systems. Our data will shed light on questions surrounding the involvement of neurotransmitters in mediating the adverse behavioral effects from Al2O3-NPs.

Close association of intestinal autofluorescence with the formation of severe oxidative damage in intestine of nematodes chronically exposed to Al(2)O(3)-nanoparticle.

In nematodes, acute exposure (24-h) to 8.1-30.6 mg/L Al(2)O(3)-nanoparticles (NPs) or Al(2)O(3) did not influence intestinal autofluorescence, whereas chronic exposure (10-d) to Al(2)O(3)-NPs at concentrations of 8.1-30.6 mg/L or Al(2)O(3) at concentrations of 23.1-30.6 mg/L induced significant increases of intestinal lipofuscin accumulation, and formation of severe stress response and oxidative damage in intestines. Moreover, significant differences of intestinal autofluorescence, stress response and oxidative damage in intestines of Al(2)O(3)-NPs exposed nematodes from those in Al(2)O(3) exposed nematodes were detected at examined concentrations. Oxidative damage in intestine was significantly correlated with intestinal autofluorescence in exposed nematodes, and oxidative damage in intestine was more closely associated with intestinal autofluorescence in nematodes exposed to Al(2)O(3)-NPs than exposed to Al(2)O(3). Thus, chronic exposure to Al(2)O(3)-NPs may cause adverse effects on intestinal lipofuscin accumulation by inducing the formation of more severe oxidative stress in intestines than exposure to Al(2)O(3) in nematodes.