Methane Dicarboxylic Aldehyde Research Articles

Trehalose suppresses cadmium-activated Nrf2 signaling pathway to protect against spleen injury

Cadmium (Cd), as a kind of ubiquitous and highly toxic heavy metal pollutants, has been known to result in immunotoxicity in animals. As a multifunctional bioactivity disaccharide, trehalose (Tre) is characterized by antioxidative, antiapoptotic, and accelerating autophagy. In this study, Sprague-Dawley (SD) rats were fed with cadmium chloride (CdCl2) and/or Tre to explore the molecular mechanisms of Tre-protected against spleen injury caused by Cd exposure. Firstly, the results showed that Tre partially recovered splenic pathological changes induced by Cd exposure. Secondly, Tre dramatically declined the level of methane dicarboxylic aldehyde (MDA) and elevated the level of total antioxidant capacity (T-AOC) to weaken oxidative stress caused by Cd exposure in spleen tissue. Moreover, the results showed that Tre significantly suppressed Cd-induced the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and up-regulated the protein expression of nuclear Nrf2. Thirdly, Tre remarkably reduced the protein expression of sequestosome 1 (p62/SQSTM1) and microtubule-associated protein light chain 3II (LC-3II) to restore autophagy inhibition induced by Cd exposure. Finally, the results of TUNEL and the expression of apoptosis marker proteins showed that Tre significantly inhibited Cd-induced apoptosis in spleen tissue to exert its protective effects. In summary, the results indicated that Tre modulated Nrf2 signaling pathway, which interacted with apoptosis and autophagy to against Cd-induced spleen injury, providing potential therapeutic strategies for the prevention and treatment of Cd-related immune system diseases.

Allicin alleviated learning and memory deficits caused by lead exposure at developmental stage

AimsIt is a promising approach to search the therapeutic strategies for treating lead (Pb) toxicity. Allicin, a natural compound extracted from Allium sativum (garlic), has been reported to have many beneficially biological properties. In this study, we investigated the protective effects of allicin on learning and memory function of rats exposed by lead acetate at developmental stage. Materials and methodsRats received lead acetate for inducing toxicity, and gavaged with allicin to ameliorate this toxicity. Morris water maze test was performed to determine learning and memory function. Superoxide dismutase (SOD), glutathione (GSH) and methane dicarboxylic aldehyde (MDA) was measured to determine oxidative stress. Immunofluorescence was carried out to analyze GFAP-positive cells. The protein expression of ERK, p-ERK, EGFR and p-EGFR were detected using western blot. Key findingsWe found that allicin ameliorated lead acetate-caused learning and memory deficits by promoting hippocampus astrocyte differentiation, which mainly through EGFR/ERK signaling. Moreover, allicin attenuated the increased ROS level by regulating the oxidative defense system. SignificanceThese results suggest that allicin is a potent agent able to ameliorate lead acetate-induced learning and memory deficits during early development, and may thus be useful for defeating lead acetate toxicity.

Macleaya cordata extract alleviated oxidative stress and altered innate immune response in mice challenged with enterotoxigenic Escherichia coli.

This study examines the effects of dietary Macleaya cordata extract (MCE) on bacterial burden and resistance to enterotoxigenic Escherichia coli (ETEC) in ICR mice. ICR mice were randomly distributed into one of the following groups: (i) basal diet; (ii) basal diet with 200 mg kg-1 MCE; (iii) basal diet challenged with ETEC; and (iv) basal diet with 200 mg kg-1 MCE and challenged with ETEC. Following a 7-day period of pre-treatment, CTRL-ETEC and MCE-ETEC mice were subjected to oral infection using 5×108E. coli SEC 470. The results showed dietary 200 mg kg-1 MCE markedly reduced intestinal ETEC burden (P < 0.05) and the disease-associated mortality was significantly alleviated in the MCE treated group (P < 0.05). In addition, dietary MCE markedly alleviated ETEC-induced oxidative stress, evidenced by the lowered methane dicarboxylic aldehyde (MDA) abundance and enhanced activities of catalase and glutathione peroxidase (P < 0.05). Furthermore, MCE mice exhibited higher immune activity, which might have further mediated ETEC infection. These results indicate MCE plays a preventative role with respect to ETEC infection. Future research should aim to develop MCE as a therapeutic approach to the promotion of intestinal health and a safeguard against ETEC infection.

Alterations in transcriptome and antioxidant activity of naturally aged mice exposed to selenium-rich rice.

Selenium (Se) is a vital element which leads to strong antioxidation in animals and humans. However, the mechanism underlying natural cereal Se-induced biological changes is not well understood. This study intended to explore the gene differential expression in naturally aged mice exposed to selenium by RNA-Seq technique. A total spectrum of 53 differentially expressed genes was quantified in mice heart tissues treated with Se-rich and general rice. The GO functional annotation of differentially expressed genes disclosed the enrichment of cellular process, ionic binding, biological regulation, and catalytic activity. One hundred twenty-three differential pathways (cardiovascular diseases, immune system, transport and catabolism, longevity regulating, and PI3K-AKT signaling) were identified according to KEGG metabolic terms. Afterwards, the effect of Se-rich rice on the antioxidant activity was assessed. The selenium-rich diet increased the total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in mice serum and livers while significantly reduces methane dicarboxylic aldehyde (MDA) contents. FOXO1 and FOXO3 genes, which acted as the regulators of apoptosis and the antioxidant enzyme, were significantly enhanced in mice when fed with Se-rich rice. In short, the present findings disclosed the alluring insights of organic and inorganic selenium sources on certain biological processes and antioxidant activity of living bodies. However, long-term trials are still required to draw a definitive conclusion, including risks and benefit analysis for various management strategies.

Treadmill Exercise Decreases Aβ Deposition and Counteracts Cognitive Decline in APP/PS1 Mice, Possibly via Hippocampal Microglia Modifications.

Recent studies have suggested that exercise may be beneficial for delaying or attenuating Alzheimer’s disease (AD). However, the underlying mechanisms were not clear. Microglia-mediated neuroinflammation is suggested to play an important role in the pathology of AD. The present study investigated the beneficial effects of treadmill exercise on amyloid-β (Aβ) deposition and cognitive function in amyloid precursor protein (APP)/PS1 mice in the early stage of AD progression and microglia-mediated neuroinflammation was mainly analyzed. The results demonstrated that 12 weeks of treadmill exercise preserved hippocampal cognitive function in APP/PS1 mice and substantially suppressed Aβ accumulation in the hippocampus. Treadmill exercise significantly inhibited neuroinflammation, which was characterized by a remarkably reduced expression of pro-inflammatory factors and increased expression of anti-inflammatory mediators in the hippocampus, resulting from a shift in activated microglia from the M1 to M2 phenotype. Treadmill exercise also attenuated oxidative stress presented by a marked reduction in methane dicarboxylic aldehyde (MDA) level and dramatically elevated SOD and Mn-SOD activities in the hippocampus. These findings suggest that treadmill exercise can effectively prevent the decrease in hippocampal-dependent cognitive function and Aβ deposits in early AD progression possibly via modulating microglia-mediated neuroinflammation and oxidative stress.

The interaction between CSE/H2S and the iNOS/NO-mediated resveratrol/poly(ethylene glycol)-poly(phenylalanine) complex alleviates intestinal ischemia/reperfusion injuries in diabetic rats.

The purpose of the experiment was to survey the therapeutic function of resveratrol (RES)-loaded poly(ethylene glycol)-poly(phenylalanine) (PEG-PPhe) on intestinal ischemia/reperfusion injury (II/RI) via the interaction between CSE/H2S and iNOS/NO compared to free RES in diabetic rats. Diabetic rats were pretreated with 20 mg/kg of RES or the RES/PEG-PPhe complex and then subjected to 1 h of ischemia and 3 h of reperfusion. Blood and intestines were collected, intestinal pathological injury was estimated, and the contents of body weight, weights of different tissues, blood glucose, serum insulin, HOMA index, serum nitric oxide (NO) and serum sulfureted hydrogen (H2S) were observed. The dry/wet intestine ratios, the activity of superoxide dismutase (SOD); the contents of methane dicarboxylic aldehyde (MDA), glutathione (GSH), H2S, and NO; and the concentrations of inducible nitric oxide synthase (iNOS) and cystathionine-γ-lyase (CSE) were observed in the intestinal tissues. A significant reduction of weights of different tissues, blood glucose, pathological damage, dry/wet ratios, MDA, NO, iNOS expression and a significant increasement of body weight, serum insulin, HOMA index, SOD, GSH, H2S, CSE expression were observed in both treatment groups. However, a greater reduction of weights of different tissues, blood glucose (7.49-13.49 mmol/L for 72 h vs. the control) and pathological damage, iNOS expression, dry/wet ratios (6.14 ± 0.29 vs. 8.51 ± 0.42), MDA (5.01 ± 0.71 nmol vs. 9.98 ± 0.67 nmol), NO (0.52 ± 0.09 μmol vs. 0.99 ± 0.08 μmol in intestinal tissue; 19.29 ± 0.89 μmol vs. 45.23 ± 1.17 μmol in serum) was observed in the RES/PEG-PPhe group relative to the I/R (P < 0.01 for all); a greater increasement of body weight, serum insulin, HOMA index, SOD (39.79±1.78 U vs. 11.84 ± 1.02 U), GSH (31.25 ± 1.19 mg vs. 10.13 ± 0.64 mg), H2S (39.52 ± 1.32 nmol vs. 13.02 ± 1.03 nmol in intestinal tissue; 9.78 ± 0.79 μmol vs. 3.11 ± 0.85 μmol in serum), CSE expression was observed in the RES/PEG-PPhe group relative to the I/R (P < 0.01 for all). In addition, aminoguanidine (AMI, iNOS inhibitor) reduced I/R injury, and dl-propargylglycine (PAG, CSE inhibitor) increased I/R injury. The interaction between CSE/H2S and the iNOS/NO-mediated resveratrol/poly(ethylene glycol)-poly(phenylalanine) complex alleviates intestinal ischemia/reperfusion injuries in diabetic rats.

Antifungal activity of an endophytic strain of Phomopsis sp. on Sclerotinia sclerotiorum, the causal agent of Sclerotinia disease

Ethyl acetate crude extract obtained from fermented cultures of Phomopsis sp. strain S4 (strain S4 extract) was effective in the control of mycelial growth and influenced to some extent sclerotia germination and the number of sclerotia formed by Sclerotinia sclerotiorum, the major agent of Sclerotinia disease. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) studies showed that in the presence of strain S4 extract, the general hyphal morphology and cells ultrastructure of S. sclerotiorum exhibited drastic changes, including hyphae shriveled and full of holes, damaged cell wall, incomplete plasma membrane, empty cells deprived of cytoplasm, and organelles. Leakage of carbohydrates in S. sclerotiorum exposed to strain S4 extract was also detected. Moreover, the methane dicarboxylic aldehyde (MDA) content increased whereas the catalase (CAT) content was lower. In addition, strain S4 extract was analyzed by gas chromatography mass spectrometry (GC-MS). Of the 86 compounds identified in the strain S4 extract the most frequent were those with a benzene ring (60.91%). These findings suggest that strain S4 extract has potential as natural antifungal agent against S. sclerotiorum and that may be due to its ability to cause oxidative damage to the pathogen cells.

The Effects of Leukocyte Filtration on Cell Salvaged Autologous Blood Transfusion on Lung Function and Lung Inflammatory and Oxidative Stress Reactions in Elderly Patients Undergoing Lumbar Spinal Surgery.

This study was designed to investigate the effects of leukocyte filtration of autologous salvaged blood on lung function, lung inflammatory reaction, and oxidative stress reaction in elderly patients undergoing lumbar spinal surgery. Sixty elderly patients undergoing lumbar spinal surgery were randomly divided into 2 groups: Leukocyte Filter group and Control group. Serum levels of inflammatory markers including white blood cell and polymorphonuclear count, neutrophil elastase, serum surfactant protein A, methane dicarboxylic aldehyde, superoxide dismutase, interleukin (IL)-6, IL-8, tumor necrosis factor-α, and respiratory function markers including dynamic respiratory system compliance, oxygenation index, and respiratory index were measured immediately before induction of anesthesia (T0), immediately before blood transfusion (T1), and 1 (T2), 6 (T3), and 12 hours (T4) after end of blood transfusion. The Leukocyte Filter group had higher dynamic respiratory system compliance at T2, oxygenation index at T2 and T3, respiratory index and superoxide dismutase at T2, T3, and T4 than those in the Control group (P<0.05). The Leukocyte Filter group had lower white blood cell, polymorphonuclear count, neutrophil elastase, serum surfactant protein A, methane dicarboxylic aldehyde, IL-6, IL-8, and tumor necrosis factor-α at T2, T3, and T4 than those in the Control group (P<0.05). There were no significant differences in adverse reactions related specifically to blood transfusion or postoperative respiratory complications within 72 hours. Salvaged autologous blood leukocyte filtration can improve ventilation, promote gas exchange and oxygenation, and inhibit lung inflammatory and oxidative stress reactions in elderly patients undergoing lumbar spinal surgery.

Trehalose alleviates cadmium-induced brain damage by ameliorating oxidative stress, autophagy inhibition, and apoptosis.

Cadmium (Cd) is a persistent environmental contaminant and induces neurotoxicity in animals. Trehalose (Tre) exhibits powerful neuroprotective effects in certain brain injury models. Herein, we revealed the specific molecular mechanism underlying the protective effects of Tre against Cd-induced brain damage in rats. Firstly, the results showed that Tre significantly ameliorated brain pathological injury induced by Cd. Secondly, Cd-induced down-regulation of total anti-oxidation capacity (T-AOC) and up-regulation of methane dicarboxylic aldehyde (MDA) in brain tissues were significantly reversed by Tre treatment. Importantly, the augmentation of nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) caused by Cd was significantly inhibited by Tre treatment. Thirdly, the levels of autophagy marker proteins were measured and the results showed that Tre significantly reversed the up-regulation of light chain 3II (LC-3II) and sequestosome 1 (SQSTM-1/p62) caused by Cd exposure. Finally, the apoptosis rate and the levels of apoptosis marker proteins including B cell leukemia/lymphoma 2 (Bcl2) and Bcl2-associated X protein (Bax) were also measured and the results showed that Cd-induced apoptosis was markedly inhibited by Tre treatment. Collectively, our data suggested that Tre exerted its neuroprotective effects by ameliorating oxidative stress, autophagy inhibition, and apoptosis induced by Cd in rat brains. In addition, the Nrf2 signaling pathway, which is continuously activated by Cd, may contribute to brain injury.

Protective Effect of Anthocyanin on Paraquat-Induced Apoptosis and Epithelial-Mesenchymal Transition in Alveolar Type II Cells.

BackgroundParaquat (PQ) can over-accumulate in alveolar epithelial cells. Anthocyanin (An) can exert anti-oxidative properties. The role of An in PQ-induced toxicity is unclear, so we aimed to explore whether An could inhibit epithelial mesenchymal transition (EMT) induced by PQ in alveolar cells.Material/MethodsAlveolar epithelial cells were treated with PQ and An with concentration gradient for 12, 24, and 48 h. The cell viability, ROS level, and apoptosis rate were determined using the Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. The lactate dehydrogenase (LDH) leakage, methane dicarboxylic aldehyde (MDA) level, glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities were determined by spectrophotometric method. The mRNA and protein expressions were detected using quantitative real-time PCR (qPCR) and Western blot, respectively.ResultsAn reduced the PQ-induced apoptosis in a dose-dependent manner. Moreover, An reduced the ratio of Bax/Bcl-2 to ROS level. We found that An suppressed the activity of LDH and MDA and improved SOD and GPX levels. Additionally, the level of PQ-induced E-cadherin was decreased by An while the expressions of vimentin, α-smooth muscle actin (α-SMA), and collagens type I (col-I) were increased. Furthermore, An inhibited the levels of transforming growth factor β1 (TGF-β1) and activin receptor-like kinase 5 (ALK5) and reduced the phosphorylation of smad2.ConclusionsOur study shows newly discovered effects of anthocyanidins on EMT and supports their chemopreventive effects in paraquat-induced apoptosis in alveolar type II cells.

Assessment of anti-diabetic activity of peanut shell polyphenol extracts.

The present study aimed to evaluate the anti-diabetic property of peanut shell polyphenol extracts (PSPEs). Diabetic rats were oral-administrated with PSPE at doses of 50, 100, and 200 mg/kg body weight (BW) per day for 28 consecutive days, with metformin (Met) as a positive control. The results showed that, similar to the Met treatment, administration of PSPE caused significant decreases in food intake, water intake, fasting blood glucose, total cholesterol, triglyceride, low-density lipoprotein cholesterol, and methane dicarboxylic aldehyde in serum, and significant increases in BW, insulin level, high-density lipoprotein cholesterol, superoxide dismutase, glutathione, and liver glycogen. Further, glucose tolerance was markedly improved in the PSPE-treated diabetic groups. Histopathological results showed that PSPE improved cellular structural and pathological changes in liver, kidney, and pancreatic islets. Collectively, the results indicated that the hypoglycemic effects of PSPE on high-fat diet/streptozotocin (HFD/STZ)-induced diabetes are comparable to Met, though their exact mechanism actions are still under investigation. Therefore, the current study suggests that PSPE could be a potential health-care food supplement in the management of diabetes.

Combination of Ginsenoside Rg1 and Astragaloside IV reduces oxidative stress and inhibits TGF-β1/Smads signaling cascade on renal fibrosis in rats with diabetic nephropathy.

IntroductionAnti-oxidative stress and inhibition of TGF-β1/Smads signaling cascade are essential therapeutic strategies for diabetic nephropathy (DN). In this study, we aimed to explore the effect of combination of Ginsenoside Rg1 and Astragaloside IV on oxidative stress and TGF-β1/Smads signaling in DN rats.Materials and methodsWistar rats were divided into five groups: N group, M group (streptozotocin [STZ], intraperitoneally), G group (STZ rats with Ginsenoside Rg1, intragastrically [ig]), A group (STZ rats with Astragaloside IV, ig) and C group (STZ rats with Ginsenoside Rg1 and Astragaloside IV, ig). The levels of methane dicarboxylic aldehyde (MDA), catalase (CAT), glutathione peroxidase (GSH-PX), total anti-oxidative capacity (T-AOC), blood urea nitrogen (BUN), β2-microglobulin (β2-MG), serum creatinine (SCr) and urinary creatinine (UCr) were detected in all the groups. The left kidneys of the rats were harvested to detect the expression of TGF-β1, Smad2/3, Smad7 and CTGF by immunohistochemical staining, while the right kidneys were used to detect the mRNA expression of TGF-β1, Smad7 and CTGF by real-time PCR.ResultsRats in G group, A group and C group had lower level of MDA but higher levels of CAT, GSH-PX and T-AOC compared with rats in M group. Rats in C group showed the best anti-oxidative stress level. G group, A group and C group treatments significantly decreased the levels of BUN, SCr, β2-MG and UCr. In addition, C group treatment showed the best kidney protective effect. G group, A group and C group treatments significantly diminish ED both factor and mRNA overexpression of TGF-β1 and CTGF but increase Smad7 expression in kidney tissue.ConclusionThe combination of Ginsenoside Rg1 and Astragaloside IV may potentially protect against DN by reducing oxidative stress and inhibiting TGF-β1/Smads signaling cascade.

The neuroprotective effect of deep brain stimulation at nucleus basalis of Meynert in transgenic mice with Alzheimer's disease

BackgroundAlzheimer's disease (AD) is the most common type of dementia and mainly treated by drugs, while the therapeutic outcomes are very limited. This study aimed to determine the optimized parameters of deep brain stimulation (DBS) which was applied to the treatment of AD and propose the involved mechanisms. MethodsAmyloid-β precursor protein/Presenilin1 (APP/PS1) transgenic mice were used and received DBS at nucleus basalis of Meynert (NBM). The optimized parameters of DBS were determined by using different stimulation frequencies, durations and ages of mice under Morris water maze test. The involved mechanisms and the possible signal pathways were also investigated. ResultsThe optimized parameters for DBS were high frequency (100 Hz) for 21 days starting from early age (4 months old). Under the above parameters, the soluble Aβ40 and Aβ42 in the hippocampus and cortex were down-regulated significantly. DBS increased survival neurons and reduced apoptotic cells in the hippocampus and cortex. Meanwhile, the apoptosis-related proteins caspase-3, caspase-8 and Bid were down-regulated. Moreover, DBS caused a significant increase of superoxide dismutase, glutathione peroxidase and choline acetyltransferase activity as well as a decrease of methane dicarboxylic aldehyde content and acetylcholine esterase activity. Phosphorylation of Akt (p-Akt)/total Akt (t-Akt) was up-regulated while p-extracellular signal-regulated kinase 1/2 (ERK1/2)/t-ERK1/2 was down-regulated. The neuroprotective effect of DBS was attenuated by their inhibitors. ConclusionsNBM-DBS starting from 4 months of age for 21 days at a high frequency (100 Hz) has therapeutic effects on AD through activating phosphatidylinositol 3′-kinase (PI3K)/Akt pathway and inhibiting ERK1/2 pathway.

Effects of cadmium exposure on expression of glutathione synthetase system genes in Acidithiobacillus ferrooxidans.

The glutathione synthetase system (GSS) is an important pathway of glutathione synthesis and plays a key role in heavy metal resistance. In this work, the response of Acidithiobacillus ferrooxidans to extracellular Cd2+ was investigated, and the interplay between Cd2+ resistance and the expression of GSS related-genes was analyzed by reverse-transcription quantitative PCR (RT-PCR). During growth in the presence of 5, 15 and 30mM Cd2+, the transcript levels of eight GSS pathway genes were affected between 0.81- and 7.12-fold. Increased transcription was also reflected in increased enzyme activities: with those of glutathione reductase (GR) increased by 1.10-, 2.26- and 1.54-fold in the presence of 5, 15 and 30mM Cd2+, respectively. In contrast, the activities of catalase (CAT) and superoxide dismutase (SOD) were decreased in the presence of Cd2+. At the metabolite level, intracellular methane dicarboxylic aldehyde (MDA) content was increased 1.97-, 3.31- and 1.92-fold in the presence of 5, 15 and 30mM Cd2+, respectively. These results suggest that Cd2+ directly inhibits the activities of CAT and SOD, breaks the redox balance of the cells, which leads to the activation of the other antioxidant pathway of GSS. Resistance of A. ferrooxidans to Cd2+ may involve modulation of expression levels of glutathione S-transferase (GST), GR, and glutathione synthetase, which may protect against oxidative damage.

Overexpression of Sedum alfredii cinnamyl alcohol dehydrogenase increases the tolerance and accumulation of cadmium in Arabidopsis

Plant cell walls protect plants from heavy metal stress by resistance, transport and the adsorption process. Cell walls are impregnated with lignin, which enables structural integrity, long-distance water transport and protects plants from many types of stress. Cinnamyl alcohol dehydrogenase (CAD) is an essential enzyme that participates in the final step of the phenylpropanoid lignin biosynthetic pathway and plays an important role in the stress resistance process. In this study, we demonstrated that a CAD-encoding gene in the hyper-accumulating Sedum alfredii Hance, SaCAD, is constitutively expressed in all tissues. While the abundance of the SaCAD transcript is affected by cadmium (Cd) stress, it is upregulated in roots, stems and leaves during Cd treatment. Overexpression of SaCAD in transgenic Arabidopsis thaliana significantly increased CAD activities. Compared with the wild type (WT) plants, the Cd concentrations of SaCAD-overexpressing plants increased in the leaves and roots under Cd stress. The increased fixation of Cd to the thickened cell wall in the SaCAD-overexpressing A. thaliana plants resulted in better growth when the plants were grown in Cd stress conditions. In agreement with these data, SaCAD-overexpressing plants exhibited higher Cd tolerance compared to the wild type (WT) with higher chlorophyll and proline (Pro) contents and antioxidant enzyme activity, as well as a lower methane dicarboxylic aldehyde (MDA) content, electric conductivity and reactive oxygen species when exposed to Cd stress due to a lower amount of Cd distributed in the cytoplasm which is the most site of cytosolic metabolism. SaCAD was found to localize to the cytoplasm of tobacco cells. NMT analysis of the root tips from transgenic A. thaliana lines during Cd stress confirmed that SaCAD-overexpressing plants were capable of retaining more Cd in the cell wall in the Cd-supplied growth medium, which provided additional evidence for the potential role of SaCAD in heavy metal ion compartmentation and detoxification. In summary, we concluded that SaCAD performs critical functions in plants: Cd absorption and fixation to lignified cell wall during stress conditions.

Homocysteine level in patients with obstructive sleep apnea/hypopnea syndrome and the impact of continuous positive airway pressure treatment.

Obstructive sleep apnea/hypopnea syndrome (OSAHS) is a common disorder in the general population. The aim of this study was to investigate the homocysteine (Hcy) level in the patients with OSAHS of varying degrees and the effect of continuous positive airway pressure (CPAP) treatment on OSAHS patients. A total of 117 OSAHS patients were recruited and divided into 3 groups (mild OSAHS, moderate OSAHS and severe OSAHS), while 33 non-OSAHS people were selected as control group. For all cases, polysomnography (PSG) variables and the concentrations of Hcy, methane dicarboxylic aldehyde (MDA) and glutathione (GSH) were recorded. Serum Hcy was measured by cyclophorase. The values of MDA and GSH were measured by a spectrophotometer. In the severe OSAHS group, a total of 30 patients received CPAP for more than 4 h every night and were re-examined 6 months later. The serum levels of Hcy, MDA and GSH showed a significant difference in OSAHS patients and controls. The Hcy and GSH concentrations of OSAHS patients with CPAP treatment showed no apparent change compared with the prior treatment, but the MDA level was obviously lower after CPAP treatment. In controls and the mild/moderate OSAHS groups, multi-element linear regression analysis results indicated that there was a statistically significant relationship between the Hcy concentration and various independent variables (age, MDA, GSH, and the apnea-hypopnea index - AHI). The change of the Hcy level was not proportional to the severity of the disease in different groups of OSAHS patients, and CPAP did not affect the Hcy levels.

Antioxidative and hepatoprotective activities of the ethyl acetate fraction separated from the fruit of Livistona chinensis

OBJECTIVETo examine the antioxidative and hepatoprotective activities of the effective fraction separated from the fruit of Livistona chinensis (FLC) and to explore the possible mechanism. METHODSThe antioxidative activities of the various fractions separated from FLC were analyzed by in vitro DPPH (1,1-diphenyl-2-picrylhydrazyl radical 2, 2-diphenyl-1-(2,4,6-trinitrophenyl) hydrazyl, DPPH) radical and superoxide anion free radical (O2 −) scavenging assays. The potential hepatoprotective effects of the ethyl acetate fraction separated from FLC (EFLC) were examined in LO2 cells and mice. LO2 cells were incubated with EFLC and exposed to H2O2-induced oxidative stress. BABL/C mice were orally administered EFLC for consecutive 7 d, and fulminant hepatitis was induced by cauda vein injection of ConA on day 7. RESULTSEFLC showed prominent antioxidative effects in DPPH - and O2 - scavenging assays. EFLC pretreatment effectively protected LO2 cells from H2O2-induced oxidative stress by decreasing apoptosis and raising the levels of antioxidant enzymes. Additionally, EFLC protected mice against ConA-induced fulminant hepatitis by markedly reducing the serum levels of alanine transaminase and aspartate aminotransferase, attenuating histological damage of the mouse liver, and elevating the levels of glutathione peroxidase and total superoxide dismutase, while decreasing the contents of methane dicarboxylic aldehyde, tumor necrosis factor-α, and interleukin-1β in the mouse liver. Furthermore, EFLC pretreatment downregulated the protein expression of B-cell lymphoma 2 (Bcl-2) associated X protein, caspase-3, caspase-8, Fas, and FasL, while upregulating the protein expression of Bcl-2 in the mouse liver. CONCLUSIONThese findings revealed that EFLC effectively protected against in vivo and in vitro liver injury, and the mechanism is closely associated with its antioxidative and anti-apoptotic properties.

Effects of dexmedetomidine on responses to tourniquet in patients undergoing lower extremity surgery with peripheral nerve block

Objective To evaluate the effects of dexmedetomidine on responses to tourniquet in patients undergoing lower extremity surgery with peripheral nerve block. Methods Eighty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients of both sexes, aged 22-63 yr, weighing 47-81 kg, scheduled for elective foot surgery under ultrasound-guided popliteal sciatic nerve block combined with saphenous nerve block, were divided into 2 groups (n=40 each) using a random number table method: control group (group C) and dexmedetomidine group (group D). Dexmedetomidine was intravenously infused for 10 min in a dose of 1 μg/kg in group D, and the equal volume of normal saline was given instead in group C. Blood samples were taken from the internal jugular vein before using the tourniquet (T0) and at 30 and 60 min after releasing the tourniquet (T1-2) for determination of the levels of c-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), methane dicarboxylic aldehyde (MDA) and superoxide dismutase (SOD) in plasma.The time to responses to tourniquet, tourniquet tolerance time and tourniquet tolerance period were recorded.The occurrence of hypotension, bradycardia and nausea and vomiting was also recorded. Results Compared with the baseline at T0, the concentrations of plasma CRP, TNF-α and MDA were significantly increased and the activity of plasma SOD was decreased at T1, 2 in the two groups (P<0.05). Compared with group C, the concentrations of plasma CRP, TNF-α and MDA were significantly decreased and the activity of plasma SOD was increased at T1, 2, the time to responses to tourniquet, tourniquet tolerance time and tourniquet tolerance period were prolonged, and the incidence of bradycardia was increased in group D (P<0.05). Conclusion Dexmedetomidine can reduce responses to tourniquet in patients undergoing lower extremity surgery with peripheral nerve block. Key words: Dexmedetomidine; Nerve block; Tourniquets; Lower extremity

Genipin attenuates hyperoxia-induced lung injury and pulmonary hypertension via targeting glycogen synthase kinase-3 β in neonatal rats.

Bronchopulmonary dysplasia is the most common chronic lung disease of infancy and is associated with pulmonary hypertension (PH). Inhibition of glycogen synthase kinase (GSK)-3 β has been shown to attenuate lung injury and PH in hyperoxia-exposed newborn rats. Genipin has been widely used for the treatment of inflammatory diseases. The aim of this study was to show that genipin decreased the expression of GSK-3 β in lung tissues of hyperoxia-exposed rat pups. We established models of hyperoxia-exposed rat pups, evaluated lung injury and pulmonary hypertension and detected the mRNA and protein expression of key molecules. Hyperoxia resulted in the reduction of survival rate and histologic injury of lung tissues; an increase of the messenger RNA (mRNA) expression of transforming growth factor-β1, extracellular matrix proteins collagen-I and fibronectin, and α-smooth muscle actin; an increase of right ventricular (RV) systolic pressure and the weight ratio of RV to left ventriclar (LV) plus septum (S) (RV/LV + S) were inhibited by genipin. Genipin also decreased the levels of tumor necrosis factor-α, interleukin-1 β, and interleukin-6 in both bronchoalveolar lavage fluid and lung tissues after hyperoxia exposure. In addition, genipin inhibited p65 nuclear factor-κB nuclear translocation and matrix metalloproteinase-2 and -9 expression. Moreover, hyperoxia resulted in an increase of methane dicarboxylic aldehyde content and a decrease of superoxide dismutase activity, catalytic subunit of glutamate-cysteine ligase, modified subunit of glutamate-cysteine ligase, and nuclear factor erythroid 2-related factor 2 expression were inhibited by genipin. All these effects induced by genipin were blocked by upregulation of GSK-3 β. Genipin downregulated GSK-3 β expression, decreased nuclear factor-κB translocation, increased nuclear factor erythroid 2-related factor 2 expression, attenuated inflammation and oxidative stress, leading to amelioration of lung injury and PH in hyperoxia-exposed rat pups. Overall, genipin may provide a novel therapeutic option for preventing and treating infants with bronchopulmonary dysplasia.

A Chinese Herbal Formula Ameliorates Pulmonary Fibrosis by Inhibiting Oxidative Stress via Upregulating Nrf2.

This study aimed to explore the protective effects of a Chinese herbal formula, Jinshui Huanxian formula (JHF), on experimental pulmonary fibrosis and its underlying mechanisms. After being treated with single dose of bleomycin (5 mg/kg) intratracheally, rats were orally administered with JHF and pirfenidone from day 1 to 42, then sacrificed at 7, 14, 28, or 42 days post-bleomycin instillation. JHF ameliorated bleomycin-induced pathological changes, collagen deposition in the rat lung and recovered pulmonary function at different days post-bleomycin instillation. In lungs of JHF-treated rats, the levels of total superoxide dismutase, catalase and glutathione were higher, and myeloperoxidase and methane dicarboxylic aldehyde were lower than those in vehicle-treated rats, respectively. Additionally, JHF inhibited the expression of NADPH oxidase 4 (NOX4) and increased the Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2) in lung tissues. In vitro, JHF and ruscogenin, a compound of Ophiopogonis Radix contained in JHF, significantly inhibited transforming growth factor β1 (TGF-β1)-induced differentiation of fibroblasts. Furthermore, JHF markedly decreased the level of reactive oxygen species in TGF-β1-induced fibroblast. In line with this, upregulation of NAD(P)H: quinone oxidoreductase 1 and heme oxygenase 1, and downregulation of NOX4 were found in JHF-treated fibroblast induced by TGF-β1. While on the other hand, Nrf2 siRNA could suppress the JHF-mediated inhibition effect on alpha-smooth muscle actin (α-SMA), and FN1 expression induced by TGF-β1 in fibroblasts. These results indicated that JHF performed remarkably therapeutic and long-term effects on pulmonary fibrosis in rat and suppressed the differentiation of fibroblast into myofibroblast through reducing the oxidative response by upregulating Nrf2 signaling. It might provide a new potential natural drug for the treatment of pulmonary fibrosis.