Sophoral flavones inhibit proliferation of cardiac fibroblasts via regulating the expression of prohibitin / 药学学报

The aim of the present study was to investigate the effect of Sophoral flavones on proliferation of cardiac fibroblasts (CFb) induced by high glucose and its underlying mechanism. Cardiac fibroblasts were exposed to different concentration of D-glucose (15, 25 and 35 mmol·L-1) at different time point (24, 48 and 72 h) in order to determine cell proliferation, and the model group was established by culturing CFb with 25 mmol·L-1D-glucose for 48 h. Sophoral flavones (12.5, 25 and 50 mg·L-1) were employed for intervention. The cell viability was measured by MTT assay, and the levels of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-2 (MMP-2), collagen Ⅰ and collagen Ⅲ were measured by ELISA. In addition, flow cytometry was employed to detect the cell cycle; while the protein expression of prohibitin (PHB) was observed via immunocytochemistry and Western blot. This animal experiment had been approved by Jilin Medical University Experiment Animal Ethics Review Committee. The results showed that 25 mmol·L-1 glucose could promote the proliferation of CFb; and the contents of TGF-β1, MMP-2, collagen Ⅰ and collagen Ⅲ in the model group were higher than that of control (P<0.05). The number of cells in S and G2 phase increased under high glucose condition. In the model group, PHB translocation occurred at 6 h and protein expression decreased at 48 h (P<0.01). Compared with the model group, 12.5-50 mg·L-1 Sophoral flavones reduced the contents of TGF-β1, MMP-2, collagen Ⅰ and collagen Ⅲ, increased the number of G1 phase cells, and increased the expression of PHB protein at 48 h (P<0.05), with no effect on the nuclear translocation of PHB. These results indicated that Sophoral flavones could prevent the proliferation of CFb induced by high glucose, the mechanism of which may be related to increasing the expression of PHB protein.

Amyloid β Protein Aggravates Neuronal Senescence and Cognitive Deficits in 5XFAD Mouse Model of Alzheimer's Disease / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Amyloid β (Aβ) has been established as a key factor for the pathological changes in the brains of patients with Alzheimer's disease (AD), and cellular senescence is closely associated with aging and cognitive impairment. However, it remains blurred whether, in the AD brains, Aβ accelerates the neuronal senescence and whether this senescence, in turn, impairs the cognitive function. This study aimed to explore the expression of senescence-associated genes in the hippocampal tissue from young to aged 5XFAD mice and their age-matched wild type (WT) mice to determine whether senescent neurons are present in the transgenic AD mouse model.</p><p><b>METHODS</b>The 5XFAD mice and age-matched wild type mice, both raised from 1 to 18 months, were enrolled in the study. The senescence-associated genes in the hippocampus were analyzed and differentially expressed genes (DEGs) were screened by quantitative real-time polymerase chain reaction. Cognitive performance of the mice was evaluated by Y-maze and Morris water maze tests. Oligomeric Aβ (oAβ) (1-42) was applied to culture primary neurons to simulate the in vivo manifestation. Aging-related proteins were detected by Western blotting analysis and immunofluorescence.</p><p><b>RESULTS</b>In 5XFAD mice, of all the DEGs, the senescence-associated marker p16 was most significantly increased, even at the early age. It was mainly localized in neurons, with a marginal expression in astrocytes (labeled as glutamine synthetase), nil expression in activated microglia (labeled as Iba1), and negatively correlated with the spatial cognitive impairments of 5XFAD mice. oAβ (1-42) induced the production of senescence-related protein p16, but not p53 in vitro, which was in line with the in vivo manifestation.</p><p><b>CONCLUSIONS</b>oAβ-accelerated neuronal senescence may be associated with the cognitive impairment in 5XFAD mice. Senescence-associated marker p16 can serve as an indicator to estimate the cognitive prognosis for AD population.</p>

Clinical observation of the carotid of patients with anterior ischemic optic neuropathy using doppler ultrasound / 国际眼科杂志(Guoji Yanke Zazhi)

AlM: To investigate the relationship between the anterior ischemic optic neuropathy ( AlON ) and the carotid artery change using doppler ultrasound.METHODS:Fifty-four cases of AlON patients and 54 cases of healthy control were observed, atherosclerotic spots were detected by the application of color ultrasound.RESULTS:ln AlON group of 54 patients, 38 cases appeared carotid atherosclerosis, accounting for 70%. The number of cases with hard plaque, soft plaque and mixed plaques were 18, 13, and 7 respectively, accounting for 33%, 24% and 13%. ln the control group, 20 cases were detected atherosclerotic change, accounting for 37%. And the number of cases with hard plaque, soft plaque and mixed plaques were 12, 5 and 3 respectively, accounting for 22%, 9%, 6%. Significant stenosis and velocity change were showed in neither AlON group nor control group. Compared with the control group, AlON group had more cases of atherosclerotic plaque, the difference was statistically significant (χ2=12. 836, P=0. 005)CONCLUSlON: The incidence of AlON is correlated with carotid atherosclerosis, and carotid ultrasonography is significantly valuable for AlON etiology and diagnosis.

The efficacy and mechanism of rhIL-11 in the management of chemotherapy-induced thrombocytopenia in acute leukemia / 中华血液学杂志

<p><b>OBJECTIVE</b>To investigate the efficacy, safety and possible mechanism of rhIL-11 in the management of chemotherapy-induced thrombocytopenia in acute leukemia.</p><p><b>METHODS</b>Thirty-two acute leukemia patients were enrolled in the study. rhIL-11 was given when platelet count dropped below 30 x 10(9)/L after chemotherapy, at 1.5 mg/d, ih, for 7-14 days or withdrawn when the increase of platelet count was more than 50 x 10(9)/L. Serum IL-11 level was determined by ELISA, IL-11R alpha gene expression by RT-PCR. Efficacy and safety data were collected and their correlation with serum IL-11 and IL-11Ralpha expression were analyzed.</p><p><b>RESULTS</b>The platelet counts on day 7 and 14 after medication were (63.40 +/- 7.24) x 10(9)/L and (98.70 +/- 9.37) x 10(9)/L for 32 patients in IL-11 group [26 complete remission (CR), 2 partial remission (PR), 4 non-remission (NR)] and (42.50 +/- 6.38) x 10(9)/L and (70.30 +/- 7.12) x 10(9)/L for the control group (20 CR, 3 PR, 5 NR). There were 10 patients who received platelet transfusion (16-32 U) in IL-11 group and 19 patients (32-48 U) in control group. Compared with the IL-11 group a delay of platelet recovery was observed in controls (P < 0.05). IL-11 was generally well tolerated. Five experienced transient atrial arrhythmia and relieved after extenuation or withdrawal. The responders' serum IL-11 level of pre-medication was (21.81 +/- 1.88) ng/L, lower than that of non-responders (P < 0.05). IL-11Ralpha level was 0.3552 +/- 0.0224, higher than that of non-responders (P < 0.05). No correlation was observed among serum IL-11, IL-11Ralpha expression, platelet count, and megakaryocyte number.</p><p><b>CONCLUSIONS</b>rhIL-11 can safely accelerate the recovery of chemotherapy-induced thrombocytopenia in acute leukemia. The serum IL-11 level and IL-11Ralpha of mononuclear cells might predict the efficacy of rhIL-11.</p>

Relationship between Unexplained Chest Distress and(or) Chest Pain in Children and Head-Up Tilt Test / 实用儿科临床杂志

0.05).Conclusions Unexplained chest distress and(or)chest pain of children may has close relationship with the autonomic disturbance.As for children with unexplained chest distress and(or)chest pain without organic cardiovascular disease,HUTT in a timely manner will contribute to diagnosis of the cause.J Appl Clin Pediatr,2009,24(1):24-25