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Background. It is widely accepted that inflammation may contribute to cognitive impairment in patients with vascular dementia (VD). Our prior clinical researches have reported that acupuncture can alleviate cognitive function in VD, but the underlying mechanisms are still unclear. The purpose of this research was to explore whether acupuncture alleviates cognitive impairment by suppressing the microRNA-93- (miR-93-) mediated Toll-like receptor (TLR) signaling pathway, which triggers inflammatory responses in the central nervous system. Methods. VD was established by permanent bilateral common carotid artery occlusion in male Wistar rats. Three days after operation, the rats began daily treatment with acupuncture for two weeks. The levels of miR-93, Toll-like receptors (TLR2 and TLR4), intracellular signaling molecules (myeloid differentiation factor 88 (MyD88) and nuclear factor-kappa B (NF-κB)), and inflammatory cytokines were subsequently detected. TLR4 colocalized with neurons, microglia, and astrocytes in the hippocampus was evaluated. Neuroinflammation and cognitive function were determined after intracerebroventricular injection of TLR4 antagonist TAK-242 or agonist lipopolysaccharide (LPS) with or without acupuncture. Results. We found that acupuncture notably repressed the expression of inflammatory cytokines in the hippocampus and plasma of VD rats. The expression of TLR4, but not TLR2, was markedly downregulated by acupuncture, accompanied by a decrease in miR-93 and MyD88/NF-κB signaling pathway activation. The overexpression of TLR4 in microglia, but not in astrocytes and neurons, was reversed by acupuncture. Furthermore, intracerebroventricular injection of TAK-242 had similar effects to acupuncture on inflammation and cognitive function, while LPS injection abolished the beneficial effects of acupuncture. Conclusions. Taken together, these findings provide evidence that acupuncture attenuates cognitive impairment associated with inflammation through inhibition of the miR-93-mediated TLR4/MyD88/NF-κB signaling pathway in experimental VD. Acupuncture serves as a promising alternative therapy and may be an underlying TLR4 inhibitor for the treatment of VD.

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This review might explain, to some extent, what an acupoint is. Further research into the identity of acupoints is warranted, and multidisciplinary methods using novel technologies may yield significant advances over existing knowledge.

Lignin is a renewable material and it is abundantly available as low priced industrial residue. Lignin-based carbon fibers are economically attractive and sustainable. In addi tion, remarkably oxidized molecule o f the lignin decreases the required time and temper ature o f the thermostabilization process compared to other carbon fiber precursors such as polyacrylonitrile (PAN); and thus, decreases the processing cost o f carbon fiber pro duction. The fraction 4 o f softwood Kraft lignin (SKL-F4) was previously shown to be spinnable via electrospinning to produce carbon nanofibers. In this paper, we character ized different Kraft lignin powders through X-ray diffraction (XRD) analysis to measure the mean size o f the ordered domains in different fractionations o f softwood and hard wood samples. According to our results, SKL-F4 has largest ordered domains among SKLs and highest hydroxyl content according to Fourier transform infrared (FTIR) anal ysis. In addition, variations in the XRD patterns during carbon nanofiber formation were studied and the peak fo r (101) plane in graphite was observed in the carbon nanofiber carbonized at 1000°C.

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Gigantol is a phenolic substance extracted from plants in the genus Dendrobium and used in traditional Chinese medicine. In the present study, we aimed to investigate the growth inhibition and apoptotic effects of gigantol on human liver cancer cells through the PI3K/Akt/NF-κB signaling pathway. HepG2 cells were treated with different concentrations of gigantol (0-150 µM) for 12, 24 and 48 h. It was found that gigantol significantly inhibited the proliferation and induced apoptosis of the HepG2 cells. The results of fluorescence micrographs showed that a 48-h treatment with gigantol induced typical apoptotic morphological features, which were consistent with the flow cytometric analysis where 20% of apoptotic cells were detected in response to gigantol treatment. In addition, western blot analysis indicated that gigantol enhanced the activities of caspase-3, PARP and p53 and downregulated the expression of p-Akt/Akt. Collectively, the present data suggest that gigantol induces growth inhibition and apoptosis of HepG2 cells via the PI3K/Akt/NF-κB signaling pathway.