Objective To investigate the effects of Pollen Typhae total flavone ( PTF) , an extract from Pollen Typhae which has the actions of activating blood and removing stasis, on inflammatory factors and insulin sensitivity in type 2 diabetic rats. Methods SD rats were used as the experimental animal. Type 2 diabetic rats induced by high fat diet plus low dose of streptozotocin were randomly divided into model group, PTF group (in the dosage of 200 mg·kg-1·d-1) , and rosiglitazone group (in the dosage of 4 mg·kg-1·d-1) . Additionally, normal control group was set up. After treatment for 4 weeks, plasma interleukin 6 ( IL-6) and tumor necrosis factor alpha ( TNF-α) levels were detected, the insulin tolerance test ( ITT) was performed, and the protein expression of suppressor of cytokine signaling-3 ( SOCS-3) in skeletal muscle was determined. Results After treatment for 4 weeks, the plasma levels of IL-6 and TNF-α, the homeostasis model of insulin resistance ( HOMA-IR) , and expression level of SOCS-3 in skeletal muscle in the model groups were significantly increased ( P﹤0.05) as compared with those in the normal control group, and insulin tolerance was also impaired in the model group ( P﹤0.05) . Compared with the model group, IL-6 level and HOMA-IR were markedly decreased in the PTF group ( P﹤0.05) , and the impaired insulin tolerance was obviously improved (P﹤0.05) . The level of SOCS-3 in the skeletal muscle of PTF group was also much lower than that of the model group and rosiglitazone group (P﹤0.05) . Conclusion PTF has effects on decreasing the levels of plasma IL-6 and SOCS-3 in the skeletal muscle and on improving insulin sensitivity in type 2 diabetic rats.

Objective To investigate the effects of Pollen Typhae total flavone (PTF) on INS-1 pancreaticβcell damage induced by palmitic acid ( PA) . Methods INS-1 pancreatic β cells were given long-term induction with PA to establish the impaired cell model, and then were intervened with PTF. Cell viability was determined by tetrazolium salt ( XTT) colorimetry. Results PA impaired the viabilities of INS-1 pancreatic β cells in concentration- and time-dependent manner, and PTF improved the impairment of INS-1 pancreatic β cells induced by PA in concentration -dependent manner. Moreover, PTF showed better improvement on the impairment when the INS-1 pancreatic β cells were impaired more seriously by PA. Conclusion PTF has effects on ameliorating the impairment of INS-1 pancreaticβcells induced by PA for long time.

Objective To study the effect of RNA interference (RNAi) on HYAL1 gene mRNA expression and the invasive potential of human breast cancer cell lines. Methods Chemically synthesized double stranded RNA (dsRNA) targeting HYAL1 was transfected into human breast cancer cell lines MDA-MB-231, MDA-MB453S, ZR-75 and ZR-75-30 using SiPORT Lipid. The transfection efficiency was observed under fluorescence confocal microscopy. Expression of HYAL1 mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). Cell penetrate matrigel capacity were determined by in vitro experiment. Results HYAL1 -siRNA effectively inhibited HYAL1 mRNA expression ( P

Objective　To explore the effect of Mp1p on host macrophages through transcriptomics combined with metabolomics. Methods Firstly, a THP-1 macrophage strain (THP-1-Mp1p+) stably expressing Mp1p was constructed using lentivirus. Secondly, using high-throughput RNA sequencing (RNA Seq) technology, the expression level of intracellular mRNA was detected in transcriptomics analysis to determine differentially expressed genes; In metabolomics analysis, metabolite identification was performed through database comparison, and pathway analysis was performed on differential metabolites to reveal potential mechanisms of action. Finally, the results of metabolomics and transcriptomics were combined for analysis, and differential metabolites and genes were analyzed to further elucidate the mechanism of action of Mp1p on macrophages. Results Transcriptome analysis showed that, compared with the negative control group, the THP-1-Mp1p+ group had a total of 1 180 differentially expressed genes (DEGs), with 345 upregulated genes and 835 downregulated genes. GO enrichment analysis of DEGs showed that there were 135 differentially expressed genes, including 105 in biological processes (BP), 28 in cellular components (CC), and 2 in molecular functions (MF). The KEGG analysis results showed that the effect of Mp1p on THP-1 macrophages was highly correlated with the TNF pathway. The metabolomic analysis found that both the blank control group and the THP-1-Mp1p+ macrophage group achieved good separation between QC samples in both positive and negative ion modes. The threshold for significant differential metabolites was set at: VIP≥1 and T-test P<0.05, resulting in the identification of 488 differential metabolites, with 230 in the positive ion mode and 258 in the negative ion mode. Pathway enrichment analysis of the identified metabolites pointed to significant enrichment in metabolic pathways. The combined analysis confirmed that the tumor necrosis factor signaling pathway, interleukin-17 signaling pathway, and NF-kappaB signaling pathway were important metabolic pathways involved. Conclusions The virulence factor Mp1p may affect host macrophages by modulating the tumor necrosis factor signaling pathway, interleukin-17 signaling pathway, and NF-kappaB signaling pathway. The findings contribute to a better understanding of the mechanisms of action of Mp1p and may offer potential directions for the selection of relevant diagnostic and therapeutic targets in the future.

Migraine is a kind of common and recurrent primary headache which can be incapacitating. The pathogenesis of migraine is complex and its clinical manifestations are diverse, which cause great obstacles to the diagnoses and treatments of migraine patients. In this paper, the literatures about migraine aura in recent years were collected and analyzed, and the different types of migraine aura symptoms were classified and summarized, so as to provide a basis for further study on the mechanism, prevention and treatment of migraine with aura.

Objective To explore the inhibitory effect of saikosonin a(SSa)on pentylenetetrazol-induced acute epilepsy seizures in a mouse model of depression and explore the mechanism mediating this effect.Methods Male C57BL/6J mouse models of depression was established by oral administration of corticosterone via drinking water for 3 weeks,and acute epileptic seizures were induced by intraperitoneal injection of a single dose of pentylenetetrazole.The effect of intraperitoneal injection of SSa prior to the treatment on depressive symptoms and epileptic seizures were assessed using behavioral tests,epileptic seizure grading and hippocampal morphology observation.ELISA was used to detect blood corticosterone levels of the mice,and RT-qPCR was performed to detect the pro-and anti-inflammatory factors.Microglia activation in the mice was observed using immunofluorescence staining.Results The mouse model of corticosterone-induced depression showed body weight loss and obvious depressive behaviors with significantly increased serum corticosterone level(all P<0.05).Compared with those with pentylenetetrazole-induced epilepsy alone,the epileptic mice with comorbid depression showed significantly shorter latency of epileptic seizures,increased number,grade and duration of of seizures,reduced Nissl bodies in hippocampal CA1 and CA3 neurons,increased number of Iba1-positive cells,and significantly enhanced hippocampal expressions of IL-1β,IL-10,TNF-α and IFN-γ.Pretreatment of the epileptic mice with SSa significantly prolonged the latency of epileptic seizures,reduced the number,duration,and severity of seizures,increased the number of Nissl bodies,decreased the number of Iba1-positive cells,and reduced the expression levels of IL-1β,IL-10,TNF-α,and IFN-γ in the hippocampus(P<0.05).Conclusion Depressive state aggravates epileptic seizures,increases microglia activation,and elevates inflammation levels.SSA treatment can alleviate acute epileptic seizures in mouse models of depression possibly by suppressing microglia activation-mediated inflammation.

Objective To explore the inhibitory effect of saikosonin a(SSa)on pentylenetetrazol-induced acute epilepsy seizures in a mouse model of depression and explore the mechanism mediating this effect.Methods Male C57BL/6J mouse models of depression was established by oral administration of corticosterone via drinking water for 3 weeks,and acute epileptic seizures were induced by intraperitoneal injection of a single dose of pentylenetetrazole.The effect of intraperitoneal injection of SSa prior to the treatment on depressive symptoms and epileptic seizures were assessed using behavioral tests,epileptic seizure grading and hippocampal morphology observation.ELISA was used to detect blood corticosterone levels of the mice,and RT-qPCR was performed to detect the pro-and anti-inflammatory factors.Microglia activation in the mice was observed using immunofluorescence staining.Results The mouse model of corticosterone-induced depression showed body weight loss and obvious depressive behaviors with significantly increased serum corticosterone level(all P<0.05).Compared with those with pentylenetetrazole-induced epilepsy alone,the epileptic mice with comorbid depression showed significantly shorter latency of epileptic seizures,increased number,grade and duration of of seizures,reduced Nissl bodies in hippocampal CA1 and CA3 neurons,increased number of Iba1-positive cells,and significantly enhanced hippocampal expressions of IL-1β,IL-10,TNF-α and IFN-γ.Pretreatment of the epileptic mice with SSa significantly prolonged the latency of epileptic seizures,reduced the number,duration,and severity of seizures,increased the number of Nissl bodies,decreased the number of Iba1-positive cells,and reduced the expression levels of IL-1β,IL-10,TNF-α,and IFN-γ in the hippocampus(P<0.05).Conclusion Depressive state aggravates epileptic seizures,increases microglia activation,and elevates inflammation levels.SSA treatment can alleviate acute epileptic seizures in mouse models of depression possibly by suppressing microglia activation-mediated inflammation.

OBJECTIVE:To systematically evaluate therapeutic efficacy of modified Shenqi dihuang decoction in the treatment of chronic glomerular nephritis. METHODS:Retrieved from Wanfang database,CNKI,VIP,CBM,Cochrane Library,Medline, EMBase and PubMed,randomized controlled trials(RCTs)about modified Shenqi dihuang decoction combined with conventional therapy and (or) other Chinese patent medicine (trial group) vs. conventional therapy and (or) other Chinese patent medicine (control group)in the treatment of chronic glomerular nephritis were collected. Meta-analysis was carried out by using Rev Man 5.3 software after literature scanning,data extraction and quality evaluation. Stata 14.0 software was used to conduct Egger test to evaluate publication bias. If publication bias existed,the effect of publication bias on outcome was further evaluated by scissor compensation. TSA v0.9 software was used for trial sequential analysis(TSA)of total efficency. RESULTS:A total of 10 RCTs were included,involving 707 patients. The results of Meta-analysis showed that total response rate of trial group [RR＝1.40,95%CI(1.22, 1.61),P＜0.001] was significantly higher than that of control group; the level of urine protein [SMD＝－1.97,95%CI(－2.92,－1.03),P＜0.001] and Scr [MD＝－28.41,95%CI(－38.95,－17.87),P＜0.001] in trial group were significantly lower than control group,with statistical significance. Publication bias test of total response rate was conducted,and results of it showed that there was publication bias,but bias did not affect the results of this study. TSA analysis showed that the evidence of Meta-analysis was false positive. CONCLUSIONS:Therapeutic efficacy of modified Shenqi dihuang decoction for chronic glomerular nephritis need to be proved by more stringent RCTs.

Objective To compare the pain management effects between painless wards with quality control circle mode and conventional pain management mode.Methods A retrospective case control study was conducted on the clinical data of 233 patients with lower limb fracture admitted from August 2015 to August 2016.There were 124 males and 109 females,aged 18-74 years [(48.3 ±3.3)years].The patients were divided into observation group (n =117) and control group (n =116) according to the pain management mode.The observation group followed the standard continuous quality improvement program and combined with professional team and patients Wechat group to implement pain management,and further measures were taken in accordance with the feedbacks.The control group adopted routine painless ward nursing model for perioperative analgesia nursing intervention.The pain score VAS,the start time of functional exercise,the compliance of rehabilitation activities,the length of hospital stay,and the healing time of fracture were compared between the two groups.Results There was no significant difference in VAS scores between the two groups at 12 hours before operation and 6 hours after operation (P ＞ 0.05).The observation group had lower VAS scores at 12 hours (3.2± 1.4),24 hours (2.8 ±0.9),48 hours (1.6 ± 0.7),and 72 hours (1.5 ± 0.8) after operation than the control group (P ＜0.05).The observation group started functional exercises earlier [(18.9 ± 0.4) hours after operation]than the control group earlier [(48.1 ± 1.7) hours after operation] (P ＜ 0.01).The observation group had a rehabilitation compliance rate of 62.6％,higher than that of the control group (17.6％) (P ＜0.05).The hospital stay [(12.18 ± 0.14) days] and fracture healing time [(97.86 ± 0.83) days] of the observation group were shorter than those of the control group (P ＜ 0.05).Conclusion The pain management model of standardized continuous quality improvement can significantly relieve pain in patients with lower limb fracture,shorten hospitalization time,bring forward the start time of functional exercise,improve the compliance of rehabilitation activities,and promote fracture healing.

This study was designed to explore the effect of DNA methyltransferase 1(DNMT1)on podocyte apoptosis and inflammatory cytokine release induced by high glucose(HG),and analyze the related molecular mechanisms.Podocyte MPC-5 cells were cultured in vitro and divided into control and HG groups.DNMT1 and SOCS1 were either silenced or overexpressed using small RNA interference technology and liposome transfection technology.The expression levels of DNMT1 and SOCS1 genes were measured using qRT-PCR.Apoptosis was assessed by flow cytometry,while ELISA was employed to determine the levels of inflammatory factors such as tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),interleukin-1β(IL-1β),and monocyte chemoattractant protein-1(MCP-1).Western blot was used to detect the expression of DNMT1,SOCS1 proteins,and the proteins involved in the Janus kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3)signaling pathway.Data showed that HG elevated MPC-5 cell apoptosis rate,the level of inflammatory factors and DNMT1 mRNA expression,and the expression of DNMT1,p-JAK2 and p-STAT3 proteins,while reduced SOCS1 mRNA and protein expression(P＜0.05).Both silencing DNMT1 and overexpressing SOCS1 resulted in reduce of MPC-5 cell apoptosis rate,inflammatory factors level,p-JAK2 and p-STAT3 proteins expression(P＜0.05).Additionally,silencing DNMT1 increased SOCS1 mRNA and protein expressions(P＜0.05).Conversely,silencing SOCS1 counteracted the effects of DNMT1 silencing on MPC-5 cell apoptosis,inflammation,p-JAK2 and p-STAT3 proteins expression.Therefore,silencing DNMT1 expression can reduce the apoptosis and inflammation of podocytes induced by HG,and its mechanism may be related to the inhibition of JAK2/STAT3 signaling pathway activation by upregulating SOCS1 expression.