Expression Levels Of MDA Research Articles

Influencing intertidal food web: Implications of ocean acidification on the physiological energetics of key species the ‘wedge’ clam Donax faba

Ocean acidification has become increasingly severe in coastal areas. It poses emerging threats to coastal organisms and influences ecological functioning. Donax faba, a dominant clam in the intertidal zone of the Bay of Bengal, plays an important role in the coastal food web. This clam has been widely consumed by the local communities and also acts as a staple diet for shorebirds and crustaceans. In this paper, we investigated how acidified conditions will influence the physiology, biochemical constituents, and energetics of Donax faba. Upon incubation for 2 months in lowered pH 7.7 ± 0.05 and control 8.1 ± 0.05 conditions, we found a delayed growth in the acidified conditions followed by decrease in calcium ions in the clam shell. Although not significant, we found the digestive enzymes showed a downward trend. Total antioxidant was significantly increased in the acidified condition compared to the control. Though not significant, the expression level of MDA and antioxidant enzymes (SOD, CAT, GST, GPX, and APX) showed increasing trend in acidified samples. Among nutrients such as amino acids and fatty acids, there was no significant difference between treatments, however, showed a downward trend in the acidified conditions compared to control. Among the minerals, iron and zinc showed significant increase in the acidified conditions. The above results suggest that the clam growth, and physiological energetics may have deleterious effects if exposed for longer durations at lowered pH condition thereby affecting the organisms involved in the coastal food web.

Shengmai injection inhibits palmitic acid-induced myocardial cell inflammatory death via regulating NLRP3 inflammasome activation

ObjectiveTo determine the protective effect of Shengmai injection (SMI) on myocardial injury in diabetic rats and its mechanism based on NLRP3/Caspase1 signaling pathway. Materials and methodsRat H9c2 cardiomyocytes were cultured in vitro, and the cell survival rate of different concentrations of palmitate acid (PA) and different concentrations of SMI were detected by CCK-8. The myocardial injury cell model was induced with PA, treated with SMI, and combined with NLRP3 specific inhibitor (MCC950) to interfere with the high-fat-induced rat H9c2 myocardial cell injury model. The cell changes were observed by Hoechst/PI staining and the expression levels of MDA, SOD, and ROS in each group were detected. The protein and gene changes of the NLRP3/Caspase-1 signaling pathway were detected by Western blot and RT-qPCR, respectively. Results200 μmol/L of PA were selected to induce the myocardial injury cell model and 25 μL/mL of SMI was selected for intervention concentration. SMI could significantly reduce MDA expression, increase SOD level, and decrease ROS production. SMI could decrease the gene expression levels of NLRP3, ASC, Caspase-1, and GSDMD, and the protein expressions of NLRP3, ASC, Cleaved Caspase-1, GSDMD, and GSDMD-N. ConclusionSMI can inhibit the high-fat-induced activation of the NLRP3/Caspase-1 signaling pathway, intervene in cardiomyocyte pyroptosis, and prevent diabetic cardiomyopathy.

Forsythiaside B inhibits cerebral ischemia/reperfusion-induced oxidative stress injury in mice via the AMPK/DAF-16/FOXO3 pathway

To study the protective effect of forsythiaside B (FB) against cerebral oxidative stress injury induced by cerebral ischemia/reperfusion (I/R) in mice and explore the underlying mechanism. Ninety C57BL/6 mice were randomized into sham-operated group, middle cerebral artery occlusion (MCAO) model group, and low-, medium and highdose (10, 20, and 40 mg/kg, respectively) FB groups. The expression levels of MDA, ROS, PCO, 8-OHdG, SOD, GSTα4, CAT and GPx in the brain tissue of the mice were detected using commercial kits, and those of AMPK, P-AMPK, DAF-16, FOXO3 and P-FOXO3 were detected with Western blotting. Compound C (CC), an AMPK inhibitor, was used to verify the role of the AMPK pathway in mediating the therapeutic effect of FB. In another 36 C57BL/6 mice randomized into 4 sham-operated group, MCAO model group, FB (40 mg/kg) treatment group, FB+CC (10 mg/kg) treatment group, TTC staining was used to examine the volume of cerebral infarcts, and the levels of ROS and SOD in the brain were detected; the changes in the protein expressions of AMPK, P-AMPK, DAF-16, FOXO3 and P-FOXO3 in the brain tissue were detected using Western blotting. In mice with cerebral IR injury, treatment with FB significantly reduced the levels of ROS, MDA, PCO and 8-OHdG, increased the activities of antioxidant enzymes SOD, GSTα4, CAT and GPx, and enhanced phosphorylation of AMPK and FOXO3 and DAF-16 protein expression in the brain tissue (P < 0.01). Compared with FB treatment alone, the combined treatment with FB and CC significantly reduced phosphorylation of AMPK and FOXO3, lowered expression of DAF-16 and SOD activity, and increased cerebral infarction volume and ROS level in the brain tissue of the mice (P < 0.01). FB inhibits oxidative stress injury caused by cerebral I/R in mice possibly by enhancing AMPK phosphorylation, promoting the downstream DAF-16 protein expression and FOXO3 phosphorylation, increasing the expression of antioxidant enzymes, and reducing ROS level in the brain tissue.

Combined application of multiple biomarkers for early auxiliary diagnosis of silicosis.

Silicosis is an important industrial health problem for those workers exposed to silica. The present study aimed to investigate the sensitivity and specificity of combined detection of biomarkers in early auxiliary diagnosis of silicosis, the risk factors of silicosis were also studied. The study sample comprised 65 workers who had clinical silicosis and 70 matched control subjects who were exposed to silica but did not have clinical silicosis. The levels of superoxide dismutase, malondialdehyde, interleukin 6 (IL-6), tumor necrosis factor-alpha, and cholinesterases in the serum of 135 subjects were measured. After completing the biochemical assays, a logistic regression model based on the above biochemical determination results was established, and the receiver operating characteristic curve was used for judging the discrimination ability of different statistical indexes. The expression levels of MDA, IL-6, and TNF-alpha in serum samples of patients with stage I silicosis and MDA and IL-6 in serum samples of patients with stage II silicosis were all significantly higher. Results from logistic regression analysis showed that ChEs were protective factors for silicosis, while age, chronic respiratory symptoms, IL-6, and MDA were risk factors. The areas under the ROC curve (AUC) were 0.86 (IL-6), 0.81 (MDA), and 0.65 (TNF-alpha or ChEs). AUC-ROC = 0.90 (95%CI:0.84-0.95). The diagnostic efficiency of IL-6 combined with MDA and TNF-alpha was better than that of any single biomarker.

Puerarin Inhibits Ferroptosis and Inflammation of Lung Injury Caused by Sepsis in LPS Induced Lung Epithelial Cells

Background: Ferroptosis is a new type of programmed cell death, which plays an important role in lung injury caused by sepsis. Studies have reported that Puerarin (Pue) can treat lung injury caused by sepsis in children, but whether it plays a role by regulating iron death has not been reported.Methods: LPS induced human alveolar epithelial cell A549 to form a model of lung injury caused by sepsis. MTT detected the effect of Pue on A549 cell viability and the effect of Pue on LPS-induced A549 cell viability. The effects of Pue on LPS-induced inflammatory cytokines TNF-α, IL-8, IL-1β in A549 cells were determined by ELISA assay. The expression level of MDA was detected by TBARS colorimetric quantitative detection kit. GSH kit was used to detect the expression of GSH in cells. The iron kit detected the total iron level and the expression level of ferric divalent ions in the cells. DCFH-DA fluorescent probe was used to detect ROS levels. Western blot was used to detect the expression of ferroptosis-related proteins in cells.Results: Pue alleviated LPS-induced injury and inflammatory response in A549 cells, and Pue reduced the expression of ROS, MDA and GSH in LPS-induced A549 cells. In addition, Pue reduced total iron levels and ferrous ion levels in LPS-induced A549 cells, and decreased the expression of iron ferroptosis-related proteins.Conclusion: Puerarin inhibited ferroptosis and inflammation of lung injury caused by sepsis in children in LPS induced lung epithelial cells.

H2S improves doxorubicin-induced myocardial fibrosis by inhibiting oxidative stress and apoptosis via Keap1-Nrf2.

OBJECTIVE: We waimed to investigate whether HS can relieve the myocardial fibrosis caused by doxorubicin through Keap1-Nrf2.METHODS: Sprague-Dawley (SD) rats were randomly divided into four groups: normal control group (Control); DOX model group (DOX); HS intervention model group (DOX+HS); HS control group (HS). DOX and DOX+HS group were injected with doxorubicin (3.0 mg/kg/time) intraperitoneally. Both of the Control group and HS groups were given normal saline in equal volume, 2 weeks later, DOX+HS and HS group were controlled with NaHS (56 mol/kg/d) through the abdominal cavity, while the Control and DOX group were injected with normal saline of the same dosage intraperitoneally.RESULTS: Myocardial injury and myocardial cell apoptosis were significantly increased, the HS content in myocardial tissue was remarkably down-regulated, the expression levels of MDA, Keap1, caspase-3, caspase-9, TNF-, IL1, MMPs and TIMP-1 in rat myocardial tissue was significantly up-regulated ( 0.05), and the expression levels of GSH, NQO1, Bcl-2 were down-regulated compared with those of control group. The above results can be reversed by the DOX+HS group. There is no statistically significant difference between the Control group and the HS control group.CONCLUSIONS: These results suggest that HS can improve DOX-induced myocardial fibrosis in rats, and the keap1/Nrf2 signaling pathway, oxidative stress, inflammation, and apoptosis may be involved in the mechanism.

The Effects Of Aerobic Exercise On Free Radical Expression In Hippocampus Of Aging Rats

PURPOSE: The effects of aerobic exercise on free radical expression in hippocampus of aging rats. METHODS: Eighty male SD rats were divided into 4 groups(n=20) at random: control group(C), D-galactose aging model group(A), pre-aging aerobic exercise intervention group (S1), aerobic exercise intervention on aging group (S2). Following a 1 week acclimation to laboratory conditions, D-gal were injected in D, S1 and S2 groups rat’s peritoneal to make aging model, the injection dosage via body weight of the rats, 100mg / kg, once a day for 6 weeks. Group C were injected the same dosage of saline. We did 1 hour per day, six times per week’s swimming training seprately before and during the injection of D-gal administration in group S1 and S2. At the end of modeling and swimming, Morris water maze was used to evaluate the spatial learning and memory function of rats; the activities of SOD, GSH PX and MDA expression in hippocampus of rats in each group were measured. All data were processed with one-way ANOVA, level of significance was set at α=0.05. RESULTS: (1) Compared with group C, group A had obvious symptoms of aging. (2)Water maze navigation trial showed that group C, S1 and S2 formed stable spatial learning and memory function on day 3 but that of group A formed on day 4; in the space exploration experiment group C reached the destination for most times, the percentage of the original site quadrant of group C was the highest, and there were significant differences between other groups (P<0.01); group S2 followed but group A and S1 were relatively low. (3) Morphological observation showed that the hippocampal neurons of rats in group A appeared derangement, deepening of cell staining and cytoplasmic edema. (4) The activities of SOD and GSH-Px in the hippocampus of group S2 were similar to group C, and the activities of group A and S1 were significantly lower than group C (P < 0.01); the expression levels of MDA were significantly down-regulated in group C, group S2 followed, and all significantly lower than those in group A and S1(P<0.05). CONCLUSIONS:Swimming in the process of aging can improve and maintain the spatial learning and memory function of brain and delay brain aging. The mechanism may be related to reduce free radical expression’s regulatio.

Association between bladder fibrosis and oxidative stress in elderly diabetic patients

Objective To investigate the association between bladder fibrosis and oxidative stress in elderly diabetic patients. Methods In this study, 30 elderly patients with bladder fibrosis related diabetes treated in our hospital from June 2017 to December 2017 were selected as the research object (observation group, n=30), and the healthy population (control group 1, n=30) and non bladder fibrotic senile diabetes mellitus (control group 2, n=30) in our hospital during the same period were used as control. Fasting blood glucose, postprandial 2H blood glucose and glycosylated hemoglobin were detected. Bladder dysfunction, urodynamic indexes and oxidative stress indexes were compared between the three groups. Multivariate logistic regression analysis was used to analyze the correlation between serum oxidative stress index and bladder fibrosis in elderly diabetic patients. Results The fasting blood glucose, postprandial blood glucose and glycosylated hemoglobin of control group 2 and observation group were higher than those of control group 1 (P 0.05). The incidence of unstable bladder, low compliance bladder and bladder depression in the observation group was higher than that in the control group 1 and the control group 2 (P<0.05). The maximal urine flow rate and detrusor contraction pressure in the observation group were lower than those in the control group 1 and the control group 2, and the residual urine volume was higher than that in the control group 1 and the control 2 group (P<0.05). The maximum bladder volume, initial urinary bladder capacity and average bladder capacity in the observation group were higher than those in the control group 1 and the control group 2 (P<0.05). The expression level of CAT and SOD in the observation group was lower than that of the control group 1 and the control 2 groups (P<0.05). The expression level of MDA was higher than that of the control group and the control group (P<0.05), and the expression level of CAT and SOD in the control group was lower than that of the control group (P<0.05), and the level of MDA expression was higher than that of the control group 2 (P<0.05). Multivariate logistic regression analysis showed that the expression levels of CAT, SOD and MDA were correlated with the incidence of bladder fibrosis related senile diabetes mellitus (P<0.05). Conclusions Bladder dysfunction in elderly patients with bladder fibrosis has some obstacles, abnormal urodynamic indexes and abnormal expression of oxidative stress indicators. Key words: Diabetes Mellitus; Aged; Urinary Bladder; Fibrosis; Oxidative Stress

Protective effects of genipin on ethanol-induced acute gastric injury in mice by inhibiting NLRP3 inflammasome activation

Genipin has been shown to exert anti-inflammatory effects, but its mechanism in protecting the ethanol-induced acute gastric injuries remains largely unclear. The present study aimed to investigate the effects of genipin on ethanol-induced acute gastric injuries in mice. After intragastrical administration of genipin for 7 consecutive days, acute gastric injuries were induced in the mice by ethanol treatment for 1 h. The expression levels of MDA, MPO, SOD, CAT, and NO in gastric tissues, and the levels of IL-6, TNF-α, MTL, SP, VIP and SS in serum samples were measured by ELISA. In addition, Western blotting was used to determine the expression levels of proteins involved in NLRP3 signaling pathway. The findings revealed that oral administration of genipin significantly ameliorated the pathological injury of gastric mucosa induced by ethanol, decreased the oxidative stress induced by ethanol and suppressed the expression levels of in-flammatory cytokines in gastric tissues and serum samples. In addition, it was observed that oral administration of genipin could remarkably inhibit the expression levels of related proteins in the NLRP3 signaling pathway. In conclusion, these results suggest that genipin may exhibit protective roles in ethanol-induced gastric mucosal injuries by activating antioxidant system and attenuating inflammatory reaction.

Silica nanoparticles trigger the vascular endothelial dysfunction and prethrombotic state via miR-451 directly regulating the IL6R signaling pathway

BackgroundSafety evaluation is a prerequisite for nanomaterials in a wide range of fields, including chemical industries, medicine or food sciences. Previously, we had demonstrated that SiNPs could trigger the thrombotic effects in vivo, but the underlying mechanisms remain unknown. This study was aimed to explore and verify the role of miR-451a on SiNPs-induced vascular endothelial dysfunction and pre-thrombotic state.ResultsThe color doppler ultrasound results showed that SiNPs had the inhibitory effects on aorta velocity and cardiac output. The histological and ultrastructural analysis manifested that SiNPs could induce the vascular endothelial damage. In addition, the expression level of MDA was elevated while the activity of SOD and GSH-Px were decreased in aortic arch triggered by SiNPs, accompanied with the release of iNOS and decline of eNOS in blood serum. The immunohistochemistry results showed that the positive staining of TF and PECAM-1 were elevated in a dose-dependent manner induced by SiNPs. The activation of coagulation function occurred via shortened TT, PT and APTT while the FIB was elevated markedly induced by SiNPs. Coagulant factors (TF, FXa and vWF) and PLT numbers were increased whereas the levels of anticoagulant factors (ATIII, TFPI and t-PA) were decreased. Microarray analysis showed that the down-regulated miR-451a could target the gene expression of IL6R, which further activated the JAK/STAT signaling pathway triggered by SiNPs. Dual-luciferase reporter gene assay confirmed the directly target relationship between miR-451a and IL6R. Additionally, the chemical mimics of miR-451a led to attenuate the expression of IL6R/STAT/TF signaling pathway in vitro and in vivo induced by SiNPs, while the inhibitor of miR-451a enhanced the activation of IL6R/STAT/TF signaling pathway.ConclusionsIn summary, SiNPs could accelerate the vascular endothelial dysfunction and prethrombotic state via miR-451a negative regulating the IL6R/STAT/TF signaling pathway.

L-3-n-butylphthalide attenuates cognitive deficits in db/db diabetic mice.

Numerous epidemiological studies have shown that diabetes mellitus (DM) is associated with dementia and cognition decline. However, there is currently no effective treatment for diabetes-induced cognitive dysfunction. The neuroprotective effect of L-3-n-butylphthalide (L-NBP) has been demonstrated in vascular dementia animal models. The purpose of this study was to determine whether L-NBP can ameliorate cognitive deficits in db/db mice, a model of obesity and type 2 diabetes. The mice were administered with vehicle or L-NBP (120mg/kg) by gavage daily for 6weeks. Then, Morris water maze tasks were performed, and hippocampal LTP was recorded in vivo. Next, the synaptic structure of the CA1 hippocampus region was investigated via electron microscopy. Finally, the expression levels of MDA, SOD, 8-OHdG, and NADPH oxidase subunits gp91 and p67, as well as the expression of NF-κB p65, TNF-α, IL-1β and caspase-3 were measured by Western blot, RT-PCR and ELISA. Treatment with L-NBP significantly attenuated the learning and memory deficits in db/db mice. Concomitantly, L-NBP also increased hippocampus synaptic plasticity, characterized by an enhanced in vivo LTP, and suppressed oxidative stress, as indicated by increased SOD activity and decreased MDA, 8-OHdG, and NADPH oxidase subunits p67 and gp91. L-NBP also significantly decreased NF-κB p65, TNF-α, IL-1βand caspase-3 levels in the hippocampus. L-NBP significantly ameliorated cognitive decline in type 2 diabetic mice, and this effect was accompanied by an improvement in hippocampal plasticity and an amelioration of oxidative stress, inflammation and apoptosis cascades. Thus, L-NBP may be a promising therapeutic agent against DM-mediated cognitive dysfunction.

Expression of Monstera deliciosa agglutinin gene (mda) in tobacco confers resistance to peach-potato aphids

The aphid is one of the most serious pests that causes damage to crops worldwide. Lectins from Araceae plant had been proved useful to control the aphid. Herein, the full-length cDNA of Monstera deliciosa agglutinin (mda) gene was cloned and then introduced into tobacco and the influence of the expression of mda in transgenic tobacco against peach-potato aphids (Myzus persicae) was investigated. Among 92 regenerated plants, 59 positive tobacco lines were obtained. Real-time PCR assays and aphid bioassay test revealed that there is a positive correlation between the expression level of mda and the inhibitory effect on peach-potato aphids. The average anti-pests ability of mda transgenic tobacco was 74%, which was higher than that of other reported lectins from Araceae plant. These results indicated that MDA is one of promising insect resistance proteins selected for the control of peach-potato aphids.