Objective To investigate the expression of brain-derived neurotrophic factor (BDNF) after intragastric administration of icariin to senescence-accelerated mice (P8 strain).Methods A total of 20 healthy male senescence accelerated mouse P8 (SAMP8) mice aged 6 months and 10 senescence accelerated mouse/resistance (SAM-R) mice with the same age were divided into model,blank,and icariin groups.Mice in the icariin group were intragastrically administered icariin in a 0.5％ sodium carboxymethyl cellulose suspension (0.01 ml/g).Mice in the model control and normal control groups were intragastrically administered 1 ml of double distilled water.Intragastric administration was done once a day in each group,for eight consecutive weeks.Spatial learning and memory abilities were detected by Morris water maze test,Expression of BDNF in mouse brain tissue was determined by immunohistochemistry and Western blot assay.Results At 8 weeks after intragastric administration of icariin to senescence-accelerated mice (P8 strain),Morris water maze results showed that escape latency was shortened (P ＜ 0.05),and the number of platform crossings was increased (P ＜ 0.05).Immunohistochemical staining and Western blot assay showed significantly increased levels of BDNF (P ＜ 0.05).Conclusions These results suggest that icariin upregulates brain-derived neurotrophic factor and improves learning and memory functions in hippocampus of the senescence-accelerated mouse.

Objective:To detect the expression of long non-coding RNA (LncRNA) ARAP1-AS1 in pancreatic cancer, and to preliminarily explore its effects on the biological behaviors of proliferation, apoptosis, migration and invasion of pancreatic cancer cell.Methods:The pancreatic cancer tissue specimens and corresponding paracancerous tissue specimens of 25 patients were collected, and the expression of ARAP1-AS1 was detected by qPCR. Human pancreatic cancer cell line PANC-1 was cultured in vitro and divided into control group, siRNA-control group (transfected with siRNA control sequence), knockout group (transfected with ARAP1-AS1 siRNA), pcDNA3.1-control group (transfected with pcDNA3.1) and overexpression group (transfected with pcDNA3.1-ARAP1-AS1), qPCR method was used to detect the transfection efficiency, CCK-8 method was used to detect the cell proliferation ability, flow cytometry was used to detect the cell apoptosis, scratch test was used to detect the cell migration ability, Transwell method was used to detect the cell invasion ability, Western blot (WB) method was used to detect the expression of proliferating cell nuclear antigen (PCNA), B lymphoma-2 protein (Bcl-2), Bcl-2 related X protein (Bax), matrix metalloproteinase-9 (MMP-9) proteins.Results:The expression level of ARAP1-AS1 in pancreatic cancer tissues was significantly higher than that in adjacent tissues (2.26±0.13 vs 1.00±0.00) ( P<0.05). Compared with the siRNA-control group, the ARAP1-AS1 level (1.01±0.02 vs 0.29±0.03), PCNA, Bcl-2, MMP-9 protein levels, cell OD value (0.57±0.05 vs 0.23±0.03), scratch healing rate (78.53±7.02 vs 48.60±5.26), and number of invasions (229.63±22.59 vs 104.25±15.04) in PANC-1 cells of the knockout group were significantly reduced ( P<0.05), the Bax protein level and the apoptosis rate (4.52±0.42 vs 32.40±1.84) were significantly increased ( P<0.05). Compared with the pcDNA3.1-control group, the ARAP1-AS1 level (1.02±0.03 vs 2.06±0.08), PCNA, Bcl-2, MMP-9 protein levels, cell OD value (0.57±0.05 vs 0.90±0.08), scratch healing rate (77.65±6.67 vs 91.22±7.34), and number of invasions (225.34±19.65 vs 327.50±25.40) in PANC-1 cells of the overexpression group were significantly increased ( P<0.05), the Bax protein level and the apoptosis rate (4.58±0.48 vs 2.29±0.24) were significantly reduced ( P<0.05) . Conclusion:LncRNA ARAP1-AS1 is highly expressed in pancreatic cancer, which can promote the proliferation, migration and invasion of pancreatic cancer cells PANC-1, and reduce cell apoptosis.

Ischemic stroke is one of the important causes of disability and death among middle-aged and elderly people in China,and there are many complicated problems from diagnosis to treatment.At present,vascular recanalization has become the most important treatment for ischemic stroke.However,the prognosis of patients is still not ideal after vascular recanalization treatment alone.At the same time,the therapeutic effect of neuroprotective drugs targeting a single target is still not significant.Annexin A5 has many biological functions,such as anticoagulation,anti-inflammation,protection of neuron survival and so on,and can be used for neuroprotective therapy such as reducing reperfusion injury after cerebral vascular recanalization.Annexin A5 can be used in the diagnosis of stroke and the construction of targeted vectors because of its close binding with phosphatidylserine.The authors summarized the multiple functions of Annexin A5,and analyzes its possible effects on ischemic stroke,so as to provide reference for the follow-up study.

Fibrosis is one of the key factors that lead to the immune exclusion of solid tumors. Although degradation of fiber is a promising strategy, its application was still bottlenecked by the side effects of causing metastasis, resulting in the failure of immunotherapy. Here, we developed an antimetastatic polymer (HPA) for the delivery of chemo-drug and antifibrotic siPAI-1 to form the nano-permeator. Nano-permeator shrank after protonation and deeply penetrated into the tumor core to down-regulate the expression of PAI-1 for antifibrosis, and further promoted the sustained infiltration and activation of T cells for killing tumor cells. Moreover, metastasis after fiber elimination was prevented by multivalent CXCR4 antagonistic HPA to reduce the attraction of CXCL12 secreted by distant organs. The administration of stroma-alleviated immunotherapy increased the infiltration of CD8⁺ T cells to 52.5% in tumor tissues, inhibiting nearly 90% metastasis by HPA in distant organs. The nano-permeator reveals the mechanism and correlation between antifibrosis and antimetastasis and was believed to be the optimizing immunotherapy for solid fibrotic tumors.