To study the mechanism of antiarthritis effects of Qufengshi Prescription.Adjuvant arthritis (AA) was applied as pathological model of rheumatoid arthritis and prednisone was used as positive control.The Prescription at high and medium dosages significantly decreased the rising level of hydrogen peroxide and interleukin-1 in AA rats (P < 0.05), the potency being similar to prednisone.Qufengshi Prescription Could reduce the rising level of interleukin-1 and hydrogen peroxide in AA rats, which may be part of mechanism of the antiarthritis effect.
To observe the effect of Tripterygium wilfordii polycoride (TWP) on ulcerative colitis (UC), and its intervention effect on toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway, thus to investigate its possible mechanism.Trinitrobenzene sulfonic acid (TNBS)/ethanol enema method was used to set up the UC rat model. With random number table, 90 male Wistar rats were divided into normal control group, model group, TWP low, medium and high dose group (3, 6, 12 mg/kg, respectively) and azathioprine (AZA) group (6 mg/kg), with 15 rates in each group. Four days after enema, rates in each group were given corresponding drug lavage for 14 consecutive days. Disease activity index (DAI), colon gross morphological damage and histological grading of each group were observed. Using Western blot and reverse transcription (RT)-PCR method, the TLR4/MyD88 signaling pathway-related proteins in UC rat intestinal tissue were detected, namely TLR4, MyD88, tumor necrosis factor receptor related factor 6 (TRAF-6), nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β).The DAI, colon gross morphological damage, and histological grading of the model group were significantly higher than that of the normal control group (all P<0.01), indicating successful establishment of UC model. The DAI, colon gross morphological damage and histological grading of the TWP high dose group were lower than those of the model group (0.87±0.25 vs 1.60±0.76, 3.93±1.94 vs 5.40±2.21, 5.45±2.73 vs 13.27±3.50, P<0.05). Compared with the normal control group, the mRNA and protein expressions of TLR4, MyD88, TRAF-6, NF-κB, TNF-α, and IL-1β in the model group rats were significantly increased (all P<0.01); which were significantly decreased in the TWP high dose group compared with model group rats (mRNA: 2.166±0.475 vs 5.647±0.275, 1.295±0.087 vs 3.774±0.418, 1.125±0.188 vs 2.535±0.320, 1.201±0.152 vs 2.082±0.077, 1.525±0.218 vs 3.094±0.022, 1.797±0.257 vs 17.152±0.145; protein: 0.252±0.010 vs 0.277±0.008, 0.172±0.002 vs 0.213±0.005, 0.233±0.006 vs 0.248±0.003, 0.099±0.003 vs 0.122±0.007, 0.238±0.002 vs 0.252±0.005, 0.235±0.003 vs 0.245±0.006, all P<0.05), also decreased in the AZA group (all P<0.01); and there were no significant differences between the TWP high dose group and the AZA group (all P>0.05).TWP can alleviate intestinal inflammation, promote healing of mucosa, showing a therapeutic effect for UC. One of its mechanisms may be through inhibiting the expression of TLR4, affecting the expression of TRAF-6, which is downstream to MyD66 signaling pathway, thus to suppress the activation of NF-κB and reduce the release of inflammatory factor such as TNF-α and IL-1β.
Anti-G equipment needs to be evaluated using human centrifuge before further developed. However, there isn't a general specification for human centrifuge evaluation of anti-G equipment. From related literature and from our over thirty years experience in this area, we sum up to five aspect technical consideration below: human centrifuge, medical specification for using human in +Gz stress experiment, anti-G equipment experimental assembly, principle should be abided by during human centrifuge evaluation of anti-G equipment. We hope that the technical considerations mentioned in the paper should be helpful to the work of setting up a specification for human centrifuge evaluation anti-G equipment. After we have a specification, the research will be conducted orderly and the anti-G [correction of an-G] equipment will be developed sequentially.
Abstract Growth hormone deficiency (GHD) diagnosis still lacks a gold standard or ideal diagnostic marker. Unlike other epigenetic mechanisms, non-coding RNAs regulate post-transcriptional levels. The information on non-coding RNAs in the field of GHD is limited. Therefore, this study aimed to explore the role of hsa_circ_0002473 as a competitive endogenous RNA for has-miR-4645-3p in attenuating the inhibitory effect of has-miR-4645-3p on SSTR2. In this study, we screened three significantly expressed circular RNAs (circRNAs) in five children with GHD, and selected the highest expressed hsa_circ_0002473 as the study object, and screened has-miR-4645-3p, which is the most likely to bind to hsa_circ_0002473, according to the microRNA (miRNA)-circRNA regulatory network, to study the role and mechanism of has-miR-4645-3p as a competitive endogenous RNA of has-miR-4645-3p on GH3 cells. Somatostatin receptor 2 (SSTR2) inhibits GH3 cell proliferation, and miRNA binding to SSTR2 inhibits the latter expression. Both bioinformatics and dual-luciferase reporter analyses showed targeting relationships between hsa_circ_0002473 and has-miR-4645-3p and between has-miR-4645-3p and SSTR2. We constructed the hsa_circ_0002473/has-miR-4645-3p axis and transfected it into GH3 cells and found that overexpression of hsa_circ_0002473 inhibited the proliferation and growth hormone (GH) secretion of GH3 cells, and that hsa-miR-4645-3p promoted the proliferation and GH secretion of GH3 cells by targeting SSTR2. Co-culture revealed that the inhibitory effect of hsa_circ_0002473 was reversed by has-miR-4645-3p. In conclusion, our findings suggest that hsa_circ_0002473 can act as a competitive endogenous RNA for has-miR-4645-3p to regulate GH3 cell proliferation and secretion by targeting SSTR2.
The morbidity and mortality rates of neonatal sepsis are high, with significant differences in risk factors and disease burden observed between developing and developed countries.
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