Association between IL-1ß polymorphisms and gastritis risk: A meta-analysis.

BACKGROUND: Helicobacter pylori (H. pylori) infection of the human stomach regularly leads to chronic gastric inflammation. The cytokine gene interleukin (IL)-1ß has been implicated in influencing the pathology of inflammation induced by H. pylori infection. Currently, several studies have been carried out to investigate the association of IL-1ß-511 (rs16944) and IL-1ß-31 (rs1143627) polymorphisms with gastritis risk; however, the results are inconsistent and inconclusive. To assess the effect of IL-1ß polymorphisms on gastritis susceptibility, we conducted a meta-analysis. METHODS: Up to March 15, 2016, 2205 cases and 2289 controls were collected from 12 published case-control studies. Summarized odds ratios and corresponding 95% confidence intervals (CIs) for IL-1ß-511 and IL-1ß-31 polymorphisms and gastritis risk were estimated using fixed- or random-effects models when appropriate. Heterogeneity was assessed by chi-squared-based Q-statistic test, and the sources of heterogeneity were explored by subgroup analyses and logistic meta-regression analyses. Publication bias was evaluated by Begg funnel plot and Egger test. Sensitivity analyses were also performed. RESULTS: The results provided evidences that the single nucleotide polymorphisms (SNPs) in IL-1ß-31 might be associated with the gastritis risk, especially in the Caucasian population, while SNPs in the IL-1ß-511 might not be. CONCLUSION: Our studies may be helpful in supplementing the disease monitoring of gastritis in the future, and additional studies to determine the exact molecular mechanisms might inspire interventions to protect the susceptible subgroups.

The effects of poloxamer 188 on the autophagy induced by traumatic brain injury.

Poloxamer 188 (P188) has been reported to reseal plasma membranes and attenuate TBI-induced neuronal death by suppressing apoptosis. Recent studies also confirm increased autophagy after traumatic brain injury (TBI). The present study aimed to investigate the effects of plasmalemmal resealing by P188 on neuronal autophagy in TBI. Scratch test was performed in rat cell line PC-12 in vitro, followed by immunofluorescence analysis of LC3 24h after PC-12 cell stretch-injury in vitro. CD1 mice were randomized into saline and P188-treatment groups (both undergoing intravenous injection of 4mg/ml, 100µl via the caudal vein 30min after TBI) as well as sham group. To analyze the effect of P188 on autophagy, the LC3 protein levels were assessed by western blotting 1h, 6h, 12h, 24h, and 48h after TBI. The autophagy-associated protein levels of Beclin-1, Bcl-2, and p62 were likewise determined. In vitro, the scratch test showed that the wound healing rate was significantly improved at 12h and 24h in P188 groups, and LC3 immunofluorescence analysis indicated that P188 induced extensive formation of LC3 puncta in PC-12 cells. In vivo, western blotting analyses revealed elevations of the LC3-II/LC3-I and Beclin-1/bcl-2 ratios as well as downregulation of p62 in the saline group, in contrast with the more significant increases of LC3-II/LC3-I and Beclin-1/bcl-2 ratios and the further downregulation of p62 in P188-treated group. These results revealed that plasma membranes were resealed after TBI, in which P188 aggravated autophagy in vivo.

Apelin-13 as a novel target for intervention in secondary injury after traumatic brain injury.

The adipocytokine, apelin-13, is an abundantly expressed peptide in the nervous system. Apelin-13 protects the brain against ischemia/reperfusion injury and attenuates traumatic brain injury by suppressing autophagy. However, secondary apelin-13 effects on traumatic brain injury-induced neural cell death and blood-brain barrier integrity are still not clear. Here, we found that apelin-13 significantly decreases cerebral water content, mitigates blood-brain barrier destruction, reduces aquaporin-4 expression, diminishes caspase-3 and Bax expression in the cerebral cortex and hippocampus, and reduces apoptosis. These results show that apelin-13 attenuates secondary injury after traumatic brain injury and exerts a neuroprotective effect.

The neuroprotective effect of apelin-13 in a mouse model of intracerebral hemorrhage.

Adipocytokine apelin-13 is a peptide which could reportedly protect the brain against ischemic reperfusion injury and traumatic brain injury (TBI). Whether apelin-13 has any roles to play in intracerebral hemorrhage (ICH) has not been clarified. We aimed to investigate the roles of apelin-13 in ICH and effects on ICH-induced apoptosis. Firstly, CD-1 mice were subjected to infusion of Type IV collagenase (to induce ICH) or saline (for shams) into the left striatum. ICH animals received intracerebroventricular administration of vehicle, apelin-13 (50µg dissolved in 5µl saline) immediately after ICH. The motor function and the cerebral water content (CWC) as well as blood brain barrier (BBB) disruption were measured, coupled with determination of ICH-induced neural cell death by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL). The apoptosis-associated proteins caspase-3 and Bcl-2 as well as the brain edema-associated proteins aquaporin-4 (AQP4) and MMP-9 were all assessed with western blotting. The results showed that apelin-13 decreased CWC and reduced Evans blue leakage into injured hemispheres, with the motor function significantly improved. Additionally, apelin-13 also acutely decreased the number of ICH-induced TUNEL-positive (TUNEL(+)) cells at 48h after ICH. The expressions of AQP4, MMP-9, caspse-3 and Bcl-2 were all downregulated by apelin-13 at 24h and 48h after ICH. All these results revealed that apelin-13 attenuated brain edema and reduced cellular death by suppressing apoptosis after ICH in mice.

[The relationship between the degradation of actin and the postmortem interval in rats].

OBJECTIVE: To observe the degradation of actin in cardiac muscle, brain and skeletal muscle of rats after death and to find an objective parameter interval (PMI) estimation. METHODS: Twenty eight clear Sprague Dawley rats put into an artificial climate incubator (set at 20 degrees C) for 0, 24, 48, 72, The actin contents in the above tissues were quantitated by Western-blot Pro Plus 5.0 image analysis system, and were then statistically analyzed RESULTS: Actin content in all these tissues decreased gradually with prolonged differences between the groups was statistically significant (P < 0.05), with fastest, then the lung, the spleen, the liver, the kidney, the cardiac muscle order. There was a strong correlation between actin degradation and determination (R2) exceeded 0.75 in all these tissues. CONCLUSION: degradation, the actin contents in cardiac muscle, liver, spleen, lung, kindey, rats decreased gradually with prolonged PMI, which may potentially be PMI estimation.