[Progress of researches on anti-inflammatory mechanism of acupuncture underlying amelioration of chronic respiratory diseases].

In recent years, acupuncture has gained great progress in the treatment of chronic respiratory diseases (CRD), and the clinical effect is remarkable, but its underlying mechanisms are relatively complex, with the anti-inflammatory effect being the primary aspect. Based on the literature both at home and abroad, we found that the anti-inflammatory mechanism of acupuncture mainly involves chemokines, kinase-related pathways, helper T cells, epigenetic modification, autophagy, vagal-mediated cholinergic anti-inflammatory pathway, etc. The researches on some anti-inflammatory mechanisms are still in the initial stage, the relationship among various pathways, and the key factors affecting the effect of acupuncture, such as acupoint selection, stimulation intensity and needling depth, etc. warrant further exploration in the future.

Effect evaluation of methylprednisolone plus mitochondrial division inhibitor-1 on spinal cord injury rats.

PURPOSE: To investigate the combination effect of methylprednisolone (MP) and mitochondrial division inhibitor-1 (Mdivi-1) on the neurological function recovery of rat spinal cord injury (SCI) model. METHODS: The weight-drop method was used to establish the rat SCI model; then, rats were randomized into sham group, SCI group, MP group, Mdivi-1 group and MP+Mdivi-1 group. Motor function scores were quantified to evaluate locomotor ability; HE staining was used to assess spinal cord histopathology; tissue water content, oxidative stress, tissue mitochondrial function, neurons apoptosis, and apoptosis-related protein expression were detected. RESULTS: From the third day after SCI, BBB score of the MP+Mdivi-1 group was obviously higher than the other experimental groups (p < 0.05). Compared with the SCI group, tissue water content of the Mdivi-1 group and MP+Mdivi-1 group reduced obviously (p < 0.05), mitochondrial membrane potential (MMP) level and ATP content in the Mdivi-1 group and MP+Mdivi-1 group were both higher (p < 0.05). Meanwhile, three kinds of treatment all reduced apoptosis significantly, while MP plus Mdivi-1 exhibited the best inhibition effect on apoptosis (p < 0.05). The expression levels of Drp1, cytochrome c, and caspase-3 were all upregulated obviously; Mdivi-1 could inhibit Drp1 upregulation induced by SCI; for the upregulation of cytochrome c and caspase-3, the inhibition effect of Mdivi-1 approached MP. When MP combined with Mdivi-1, there was the best inhibition effect. CONCLUSIONS: MP combined with Mdivi-1 may produce better neurological function recovery, through improving functional status of mitochondria and inhibiting lipid peroxidation in damaged tissue of SCI rats, and thus alleviating apoptosis.

[Effect of propofol on the transcription activity of endothelial nitric oxide synthase gene promoter in human umbilic vein endothelial cells induced by lipopolysaccharide].

OBJECTIVE: To observe the effect of propofol on the transcription activity of endothelial nitric oxide synthase (heNOS) gene promoter in human umbilic vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS). METHODS: heNOS gene promoter sequence (from-1 to -1600 bp) was subcloned into the Bgl II/Hind III sites of the firefly luciferase reporter gene vector, pGL2-Basic, to obtain the recombinant plasmid peNOS-Luc. peNOS-Luc, pGL2-Basic and pCMV-beta were cotransfected into HUVECs, which were treated subsequently with LPS, LPS+propofol and LPS+transforming growth factor beta1 (TGF beta 1), respectively. The relative activities (Luc/beta-gal) were determined in the cell lysates to evaluate the activity of heNOS gene promoter. RESULTS: Double restriction enzyme digestion and sequencing both confirmed successful construction of the recombinant plasmid peNOS-Luc, which could be effectively expressed in HUVECs. Upon LPS stimulation, the luciferase activity was obviously decreased, contrary to the effects of propofol and TGFb1 treatment, and between the latter two agents, TGF beta 1 produced higher transcription activity. CONCLUSION: Propofol can up-regulate the activity of heNOS gene promoter in HUVECs and affect the nitrogen monoxide production and release at the transcriptional level, which is probably one of mechanisms for propofol to ameliorate LPS-induced inflammatory reaction.