Effects of Functional Electrical Stimulation Controlled by Brain-computer Interface on Upper Limb Dysfunction in Stroke Patients / 中国康复理论与实践

Objective:To observe the effects of functional electrical stimulation (FES) controlled by brain-computer interface on upper limb motor dysfunction in stroke patients. Methods:From July, 2019 to November, 2020, 34 stroke patients hospitalized in neurological rehabilitation department were randomly divided into control group (n = 17) and experimental group (n = 17). They were treated with simple FES and FES controlled by brain-computer interface, respectively. The reaction time, joint position error of elbow joint, the scores of Fugl-Meyer Assessment-Upper Extremity (FMA-UE), modified Barthel Index (MBI) and event-related desynchronization (ERD) powers of affected upper limb were evaluated before and after intervention. Results:After intervention, the reaction time, joint position error of the elbow joint, the scores of FMA, MBI and ERD power of the affected elbow joint improved in both groups (F > 10.825, |Z| > 3.624, P < 0.05), and they were better in the experimental group than in the control group (F > 5.853, |Z| > 3.201, P < 0.05). Conclusion:FES controlled by brain-computer interface is positive on the rehabilitation of stroke patients with upper limb dysfunction.

Calenduloside E inhibits lipopolysaccharide-induced inflammatory response by inhibiting activation of ROS-mediated JAK1-stat3 signaling pathway in RAW264.7 cells / 南方医科大学学报

OBJECTIVE@#To investigate the effect of calenduloside E on lipopolysaccharide (LPS)-induced inflammatory response in RAW264.7 cells and explore the underlying molecular mechanism.@*METHODS@#CCK-8 assay was used to examine the effect of different concentrations of calenduloside E (0-30 μg/mL) on the viability of RAW264.7 cells. The release of the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in RAW264.7 cells in response to pretreatment with 6, 8, and 10 μg/mL calenduloside E for 2 h followed by stimulation with 100 ng/mL LPS was detected using enzyme-linked immunosorbent assay (ELISA). The expression levels of iNOS and COX-2 and the activation of JAK-stats, MAPKs and NF-кB signaling pathways in the treated cells were determined using Western blotting. A reactive oxygen species (ROS) detection kit was used to detect ROS production in the cells, and the nuclear translocation of the transcription factor stat3 was observed by laser confocal microscopy.@*RESULTS@#Calenduloside E below 20 μg/mL did not significantly affect the viability of RAW264.7 cells. Calenduloside E dose-dependently decreased the expression levels of iNOS and COX-2 induced by LPS, inhibited LPS-induced release of TNF-α and IL-1β, and suppressed LPS-induced JAK1-stat3 signaling pathway activation and stat3 nuclear translocation. Calenduloside E also significantly reduced ROS production induced by LPS in RAW264.7 cells.@*CONCLUSIONS@#Calenduloside E inhibits LPS-induced inflammatory response by blocking ROS-mediated activation of JAK1-stat3 signaling pathway in RAW264.7 cells.

Aloin induces apoptosis regulating the activation of MAPKs signaling pathway in human gastric cancer cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of aloin on apoptosis of human gastric cancer cells and explore the molecular mechanism.</p><p><b>METHODS</b>Gastric cancer MKN-28 and HGC-27 cells were cultured routinely in 1640 medium supplemented with 10% fetal bovine serum and 10% non-essential amino acids (for HGC-27 cells) and treated with different concentrations of aloin for different durations. The cell viability, cell nuclear morphology, and apoptotic rate of the cells were detected using CCK-8 assay, DAPI staining and AnnexinV-FITC/PI, respectively; Western blotting was used to detect the expression levels of PARP, procaspase 3 and the phosphorylation of p38, ERK and JNK. The cells were treated with specific inhibitors of p38, ERK and JNK, and the inhibitory effects on these pathways were detected with Western blotting; DAPI staining was used to detect the effects of inhibitors on apoptosis of gastric cancer cells.</p><p><b>RESULTS</b>Aloin dose-dependently inhibited the viability and induced apoptosis of HGC-27 and MKN-28 cells. Alion treatment obvious enhanced the phosphorylation of p38 and JNK but decreased ERK phosphorylation in the cells. Blocking ERK activation with the ERK inhibitor obviously enhanced aloin-induced cell apoptosis, where inhibiting p38 and JNK activation partly reversed alion-induced apoptosis in the cells.</p><p><b>CONCLUSIONS</b>Aloin induces apoptosis of human gastric cancer cells by activating p38 and JNK signaling pathways and inhibiting ERK signaling pathway.</p>