This study was aimed to analyze the bioinformatics of proteomics of rat bone marrow mesenchymal stem cells (MSCs) intervened by active principle region of Yang-Xin Tong-Mai Formula (apr-YTF). The latest versions of bioinformatics tools including DAVID (http://david.abcc.ncifcrf.gov/) and GO (http://www.geneontology.org/) were combined to assign a precise function to rat bone marrow MSCs intervened by apr-YTF. KEGG and VISANT were assigned with a precise function to rat bone marrow MSCs intervened by apr-YTF. The results showed that a total of 102 biological processes were mainly involved, with 35 cellular components and 6 molecular functions. These proteins interacted in 3 signal transduction pathways. It was concluded that the following proteins and signal transduction pathways played an important role in the process of apr-YTF inducing BMSCs differentiation into cardiomyocytes. Presenilin-1 and Presenilin-2 were in the Notch signaling pathway. And syntaxin-4 protein was in soluble N-ethylmaleimide sensitive fusion protein attachment protein (SNARE). The apr-YTF played a role on MSCs from multiple sites, with multiple links through different biological processes. The bioinformatics of proteomics can predict action mechanism of traditional Chinese medicine (TCM) from the holism concept. The validation in combination with molecularbiology was a good way for TCM modernization.

Objective:To evaluate the effect of methane on purinergic ion channel type 7 receptor (P2X 7R)/nod-like receptor protein 3 (NLRP3) signaling pathway during inflammatory responses in a rat model of spinal cord ischemia-reperfusion (I/R). Methods:Fifty-four clean-grade healthy male Sprague-Dawley rats, aged 3 months, weighing 350-380 g, were divided into 3 groups ( n=18 each) using a random number table method: sham operation group (group S), spinal cord I/R group (group I/R) and methane group (group M). Rats underwent sham operation in group S. Spinal cord ischemia was induced by occlusion of the thoracic aorta combined with controlled hypotension for 9 min, followed by reperfusion in anesthetized animals in group I/R.Methane-rich saline 10 mg/kg was intraperitoneally administered immediately after onset of reperfusion in group M. Motor sensory deficit index (MSDI) in hind limbs was measured at 12, 24 and 48 h of reperfusion.The L 3-5 segment of spinal cord was removed at 48 h of reperfusion for determination of the number of normal neurons (by Nissl staining), the number of activated microglia and expression of P2X 7R, NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), cysteine-requiring aspartate protease (caspase-1), interleukin-1beta (IL-1β) and IL-18 (by immunofluorescence staining) in anterior and posterior horns of spinal cord. Results:Compared with group S, the MSDI was significantly increased at 12, 24 and 48 h of reperfusion, and the number of normal neurons in anterior and posterior horns of spinal cord was decreased, the number of activated microglia was increased, and the expression of P2X 7R, NLRP3, ASC, caspase-1, IL-1β and IL-18 was up-regulated at 48 h of reperfusion in group I/R ( P<0.01). Compared with group I/R, the MSDI was significantly decreased at each time point of reperfusion, and the number of normal neurons in anterior and posterior horns of spinal cord was increased, the number of activated microglia was decreased, and the expression of P2X 7R, NLRP3, ASC, caspase-1, IL-1β and IL-18 was down-regulated at 48 h of reperfusion in group M ( P<0.05). Conclusion:The mechanism by which methane reduces inflammatory responses is related to inhibiting P2X7R/NLRP3 signaling pathway in a rat model of spinal cord I/R.

Objective:To evaluate the role of reactive oxygen species (ROS) /nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in desflurane preconditioning-induced reduction of lipopolysaccharide (LPS)-induced acute cerebral inflammation in rats.Methods:One hundred and twenty clean-grade healthy male Sprague-Dawley rats, aged 8-10 weeks, weighing 200-250 g, were divided into 4 groups ( n=30 each) using a random number table method: control group (group C), LPS-induced acute cerebral inflammation group (group L), desflurane preconditioning group (group D), and N-acetylcysteine plus desflurane preconditioning group (group ND). LPS 1 mg/kg was injected via the tail vein to establish the model of acute cerebral inflammation in L, D and ND groups.In group D, rats inhaled 8.2% desflurane for 1 h once a day for 5 consecutive days, and LPS was intravenously injected at 24 h after the end of the 5th inhalation.In group ND, ROS scavenger N-acetylcysteine 150 mg/kg was intraperitonealy injected at 30 min before each inhalation of desflurane, and the other treatments were similar to those previously described in group D. The expression of Nrf2 and kelch-like ECH-associated protein 1 (Keap1) in microglia and astrocytes in the hippocampal CA1 region was determined by immunofluorescence double staining before LPS injection (at 24 h after the last desflurane preconditioning). Morris water maze test was used to measure the escape latency, space exploration time spent in the original platform quadrant, and frequency of crossing the original platform at 6, 12 and 24 h after injecting LPS.The expression of NOD-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing CARD (ASC), caspase-1, interleukin-18 (IL-18) and interleukin-1beta (IL-1β) in microglia and astrocytes in the hippocampal CA1 region was determined by immunofluorescence double staining at 6, 12 and 24 h after injecting LPS.Nissl staining and immunofluorescence were used to count normal neurons and activated microglia and astrocytes in the hippocampus at 24 h after LPS injection. Results:Compared with group C, no significant change was found in the expression of Nrf2 and Keap1 in microglia and astrocytes before LPS injection ( P>0.05), and the escape latency was significantly prolonged, the space exploration time spent in the original platform quadrant was shortened, the frequency of crossing the original platform was decreased, the number of normal neurons was decreased, the number of activated microglia and astrocytes was increased, and the expression of NLRP3, ASC, caspase-1, IL-18 and IL-1β was up-regulated after injecting LPS in group L ( P<0.05). Compared with group L, the expression of Nrf2 was significantly up-regulated, and the expression of Keap1 was down-regulated before injecting LPS ( P<0.05), and the escape latency was shortened, the space exploration time spent in the original platform quadrant was prolonged, the frequency of crossing the original platform was increased, the number of normal neurons was increased, the number of activated microglia and astrocytes was reduced, and the expression of NLRP3, ASC, caspase-1, IL-18 and IL-1β was down-regulated after injecting LPS in group D( P<0.05). Compared with group D, the expression of Nrf2 was significantly down-regulated, the expression of Keap1 was up-regulated before injecting LPS ( P<0.05), and the escape latency was significantly prolonged, the space exploration time spent in the original platform quadrant was shortened, the frequency of crossing the original platform was decreased, the expression of NLRP3, ASC, caspase-1, IL-18 and IL-1β was up-regulated, the number of normal neurons was reduced, and the number of activated microglia and astrocytes was increased after LPS injection in group ND ( P<0.05). Conclusion:ROS/Nrf2 signaling pathway is involved in desflurane preconditioning-induced reduction of LPS-induced acute cerebral inflammation in rats.

ObjectiveTo explore the clinical efficacy of Huanglian Jiedutang as an adjunctive treatment for acute cerebral infarction complicated with gastric motility disorder. MethodSixty patients with acute cerebral infarction complicated with gastric motility disorder with fire toxin syndrome were randomly divided into a western medicine control group （control group） and a traditional Chinese medicine （TCM） combined treatment group （observation group）， with 30 cases in each group. The control group received basic treatment for cerebral infarction and relevant western medical symptomatic treatment based on the patients' gastrointestinal symptoms. The observation group received Huanglian Jiedutang in addition to the treatment provided to the control group. The treatment course was 7 days. Neurological deficit scores and gastrointestinal dysfunction scores were assessed in both groups before treatment and on the 4^th and 7^th days of treatment. Gastrointestinal electrographic parameters， serum citrulline （CIT）， and motilin （MTL） levels were measured in both groups before treatment and on the 7^th day of treatment. Clinical efficacy was compared between the two groups. ResultCompared with the baseline in both groups， the neurological deficit scores and gastrointestinal dysfunction scores were significantly reduced on the 4th and 7^th days of treatment （P<0.05）. The reductions in these scores were more significant on the 7^th day compared with those on the 4^th day of treatment （P<0.05）. On the 4^th and 7^th days of treatment， the observation group showed a significantly greater reduction in neurological deficit scores and gastrointestinal dysfunction scores compared with the control group （P<0.05）. On the 7th day of treatment， compared with the baseline， both groups showed a significant increase in gastric antral and gastric body electric wave amplitudes as well as serum CIT and MTL levels （P<0.05）， and there were no statistically significant differences in the frequency of gastric antral and gastric body electric waves. On the 7th day of treatment， compared with the control group， the observation group had a significant increase in gastric antral and gastric body electric wave amplitudes as well as serum CIT and MTL levels （P<0.05）， and there were no statistically significant differences in the frequency of gastric antral and gastric body electric waves. After 7 days of treatment， the total effective rate in the observation group was 90.00% （27/30）， higher than 76.67% （23/30） in the control group， but the difference was not statistically significant. ConclusionAdjunctive treatment with Huanglian Jiedutang can effectively improve the symptoms of neurological function impairment and gastrointestinal dysfunction in patients with acute cerebral infarction complicated with gastric motility disorder， increase gastric antral and gastric body electric wave amplitudes， improve gastric motility disorder， and increase serum CIT and MTL levels， thereby improving the imbalanced secretion function of the gastrointestinal tract.