Background: There is currently no effective treatment for vascular dementia (VaD). Scalp electroacupuncture (EA) has served clinically as an alternative treatment for VaD, but its mechanism is still unclear. In this study, we investigated the effect of EA at the Baihui (GV 20) and Shenting (GV 24) acupoints on spatial learning and memory ability, and the expression level of microRNA-81 (miR-81), interleukin-16 (IL-16), and postsynaptic density protein-95 (PSD-95) in the frontal cortex of VaD rats.Methods: Male Sprague-Dawley rats were randomly divided into four groups, sham, VaD, nonacupuncture (non-AP) and EA group. The VaD model was established by permanent bilateral occlusion of the common carotid arteries. Morris Water Maze was used to assess the rats' spatial learning and memory.Immunochemistry (IHC), quantitative reverse transcription polymerase chain reaction (qRT-PCR), and western blot analysis were performed to detect the expression level of miR-81, IL-16, and PSD-95. Finally, luciferase assay was used to determine the effect of miR-81 on IL-16 expression in PC12 cells. Results:The space exploration experiment of MWM showed the time and distance of the rat's activities around the platform were decreased in the EA group. Compared to the VaD and non-AP group, the number of terminal deoxynucleotidyl transferase-mediated dUDP nick-end labeling (TUNEL)-positive frontal cortical neurons was significantly decreased in EA group. The number of the PSD-95-positive cells and the miR-81 expression level in the frontal cortical in the EA group was dramatically increased in comparison with the other groups. In the PC12 cell validation experiment, IL-16 expression level was reduced under the condition of the miR-81 mimic treatment, while increased in the miR-81 inhibitor group. The PSD-95 protein level was up-regulated in the small interfering (si)RNA-IL16 group compared to the NC-IL16 groups with or without oxygen/glucose deprivation/reperfusion (OGD/R) conditions (P<0.05). However, this was abolished by miR-81 mimic. Conclusions:In VaD rats, EA may improve spatial learning and memory through miR-81/IL-16/PSD-95 pathway.

MicroRNAs (miRNAs) participate in the repair of skin trauma. Our previous study indicated that loureirin A promoted hair follicle stem cells (HFSCs) to repair skin epidermis. However, the mechanism of miRNA‐mediated regulation of loureirin A‐induced HFSC differentiation remained to be explored. In the present study, HFSCs from rat vibrissa were identified by immunofluorescence in vitro. Microarray and quantitative real time polymerase chain reaction analyses demonstrated that miR‐203a‐3p was upregulated in differentiated HFSCs induced by loureirin A. The expression of cytoskeletal keratin (CK) 5 and involucrin was promoted by miR‐203a‐3p mimics while repressed by a miR‐203a‐3p inhibitor. Smad1 was identified as a key target of miR‐203a‐3p using target prediction tools. Luciferase reporter gene test confirmed a special target association between miR‐203a‐3p and Smad1. Short interfering Smad1 was transfected into HFSCs, and the expression levels of CK5 and involucrin were upregulated. Thus, it can be inferred that miR‐203a‐3p negatively regulated the expression of Smad1 and promoted the differentiation of loureirin A‐induced HFSCs. Bone morphogenetic protein (BMP) signal inhibition and Wnt activation coregulate skin injury repair. BMP/Smad1 signaling is involved in maintaining the characteristics of HFSCs and inhibiting their differentiation. Our results showed that miR‐203a‐3p reduces Smad1 to release BMP inhibition. Taken together, miR‐203a‐3p/Smad1 is a potential therapeutic molecular target in skin wound healing, and may play an active role in wound repair and regenerative medicine.

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Eucommiae Folium (Duzhongye) is a traditional Chinese medicine with a long history of use in China. However, its quality-marker in Chinese Pharmacopoeia is poorly defined nowadays. The study, therefore, conducted an ultra-high-performance liquid chromatography coupled with hybrid quadrupole-orbitrap tandem mass spectrometry analysis to obtain accurate data. The obtained data were then compared with the authentic standards library using Xcalibur 4.1 software package and TraceFinder General Quan. Through the comparison, the study has putatively identified 26 bioactive compounds, which include 17 flavonoid derivatives (catechin, quercetin 3-gentiobioside, quercetin 3-O-β-D-glucose-7-O-β-D-gentiobioside, taxifolin, myricetin 3-O-galactoside, myricitrin, hyperoside, rutin, isoquercitrin, quercetin 3-O-β-xylopyranoside, quercitrin, isorhamnetin 3-O-β-D-glucoside, quercetin, kaempferol, S-eriodictyol, S-naringenin, and phloridzin), four caffeoylquinic acids (neochlorogenic acid, chlorogenic acid, isochlorogenic acid A, and isochlorogenic acid C), two alkaloids (vincamine and jervine), one lignan (pinoresinol), one xanthone (cowaxanthone B), and one steroid (cholesteryl acetate). Of these, flavonoid isoquercitrin is recommended as the new and additional pharmacopeia quality-marker candidate, which can not only overcome the unreliability of old quality-marker but also recognize the possible counterfeit.

Ferroptosis is a recently reported cellular apoptosis form. Screening for safe ferroptosis inhibitors and elucidation of the mechanisms have recently attracted significant attention. In this study, the ferroptosis‐inhibitory activities of gallotannin tannic acid and its parent, 1,2,3,4,6‐penta‐O‐galloyl‐β‐D‐glucopyranose (β‐PGG), were comparatively evaluated using an erastin‐mediated bone marrow‐derived mesenchymal stem cell (bmMSC) model, employing ferrostatin‐1 (Fer‐1) as a positive control. The relative inhibitory levels decreased in the following order: Fer‐1>tannic acid>β‐PGG. In the radical‐trapping assays, the relative levels decreased in the order of tannic acid>β‐PGG >Fer‐1. When mixed with ferrous ions, the UV‐visible spectra of tannic acid, β‐PGG, and Fer‐1 changed. In conclusion, natural tannic acid could undergo radical trapping and ferrous complexation pathways to inhibit ferroptosis in the bmMSCs. In contrast to Fer‐1, which utilized ferrous complexation to initiate its catalytic recycle, tannic acid mediated ferrous complexation to indirectly trap the radicals. The 3’‐O‐galloylation reaction enhanced the radical trapping and indirect radical trapping of tannic acid to enhance ferroptosis inhibition.