MiR-543-5p inhibits inflammation and promotes nerve regeneration through inactivation of the NF-κB in rats after spinal cord injury.

OBJECTIVE: The aim is to determine the efficacy and specific mechanism of microRNA-543-5p (miR-543-5p) on spinal cord injury (SCI). MATERIALS AND METHODS: The model of spinal cord injury was established in 6-week-old rats. Firstly, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the changes of miR-543-5p in the spinal cord of rats in each group after spinal cord injury. Next, we observed the alterations in nuclear factor-kappa B (NF-κB) RNA level after injection of miR-543-5p. In addition, the enzyme-linked immunosorbent assay (ELISA) was used to detect the expression of the inflammatory cytokines, and we used Western blotting to detect the protein associated with nerve regeneration at the protein levels. Finally, the Basso-Beattie-Bresnahan (BBB) rating scale was utilized to measure the recovery of hindlimbs function in rats. RESULTS: After spinal cord injury, the RNA expression of miR-543-5p in the rat spinal cord was decreased, and the RNA level of NF-κB was found to be decreased after the artificial injection of miR-543-5p. In the inflammatory expression, we found that the expression of various inflammatory mediators was also downregulated. However, the expression of nerve regeneration related factors was significantly upregulated, and it was observed that the evaluated score of the miR-543-5p group was higher than that of the SCI group within 1 month. CONCLUSIONS: MiR-543-5p inhibited NF-κB pathway and reduced the inflammatory factors, and ameliorated nerve regeneration, which ultimately promoted hindlimbs locomotor function.

beta-Carotene in breast milk and serum is increased after a single beta-carotene dose.

Normal lactating mothers were administered a single dose of 60 or 210 mg beta-carotene and changes in serum and milk retinol, alpha-tocopherol, and carotenoids were monitored for 8 d. Average serum beta-carotene concentrations increased 4.1- and 4.0-fold after the 60- and 210-mg doses, respectively. Milk beta-carotene concentrations increased 4.1- and 3.0-fold after the 60- and 210-mg doses, respectively. Maximum serum concentrations were reached 24 h after both supplements, although concentrations of milk beta-carotene continued to rise for 2-3 d. After 8 d, both serum and milk beta-carotene continued to rise for 2-3 d. After 8 d, both serum and milk beta-carotene concentrations remained about twofold higher than baseline concentrations. Increases in serum or milk beta-carotene concentrations were not dose-dependent. Initial serum and milk concentrations of beta-carotene predicted increases after supplementation, and increases in serum beta-carotene concentrations predicted those in milk. Concentrations of milk carotenoids were less than one-tenth their respective concentrations in serum. Lutein, beta-cryptoxanthin, lycopene, alpha-carotene, retinol, and alpha-tocopherol concentrations in serum or milk did not change significantly after beta-carotene supplementation. Retinol esters account for most of the retinol equivalents in the milk of well-nourished mothers. Initial and maximum concentrations of beta-carotene in serum and milk were strongly correlated for individual mothers. Collectively, the data showed that a single 60-mg supplement of beta-carotene sustained elevated beta-carotene concentrations in serum and milk for > 1 wk in normal mothers but did not affect concentrations of other major carotenoids, retinol, or alpha-tocopherol.

[Changes of the release of atrial natriuretic factor (ANF) and its gene transcription in morphine tolerance rat atrium].

Specific radioimmunoassay and molecular hybridization technique were used in the present work. Compared with the control rats, we found for the first time a significant decrease of ANF in plasma and a marked increase of ANF in atria in morphine tolerant rats. Simultaneously a raised level of ANF messenger RNA in morphine tolerant rat atria was observed. It is suggested that the biosynthesis and storage of ANF in atria be increased and its release from atria decreased in morphine tolerant rats.