Reduce Cell Damage Research Articles

Benzene, 1,2,4-Trimethoxy-5-(2-Methyl-1-Propen-1-yl) Attenuates D-galactose/AlCl3-induced Cognitive Impairment by Inhibiting Inflammation, Apoptosis, and improving Expression of Memory-Related Proteins

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by decreased learning ability and memory deficits. Our previous findings suggested that benzene, 1,2,4-trimethoxy-5-(2-methyl-1-propen-1-yl) (BTY) can ameliorate the dysfunction of GABAergic inhibitory neurons associated with neurological diseases. On this basis, we investigated the neuroprotective effect of BTY on AD and explored the underlying mechanism. This study included in vitro and in vivo experiments. BTY could maintain cell morphology, improve cell survival rate, reduce cell damage, and inhibit cell apoptosis in vitro experiments. Further, BTY has good pharmacological activity in vivo experiments, of which behavioral experiments showed that BTY could improve AD-like mice’s learning and memory abilities. Besides, histopathological experiments indicated that BTY could maintain the morphology and function of neurons, reduce amyloid β-protein 42 (Aβ42) and phosphorylated tau (p-tau) accumulation, and decrease the levels of inflammatory cytokines. Finally, western blot experiments showed that BTY could inhibit the expression of apoptosis-related proteins and promote the expression of memory-related proteins. In conclusion, this study indicated that BTY may be a promising drug candidate for AD.

Genome-wide identification and analysis of TCP family genes in Medicago sativa reveal their critical roles in Na+/K+ homeostasis

BackgroundMedicago sativa is the most important forage world widely, and is characterized by high quality and large biomass. While abiotic factors such as salt stress can negatively impact the growth and productivity of alfalfa. Maintaining Na+/K+ homeostasis in the cytoplasm helps reduce cell damage and nutritional deprivation, which increases a salt-tolerance of plant. Teosinte Branched1/ Cycloidea/ Proliferating cell factors (TCP) family genes, a group of plant-specific transcription factors (TFs), involved in regulating plant growth and development and abiotic stresses. Recent studies have shown TCPs control the Na+/K+ concentration of plants during salt stress. In order to improve alfalfa salt tolerance, it is important to identify alfalfa TCP genes and investigate if and how they regulate alfalfa Na+/K+ homeostasis.ResultsSeventy-one MsTCPs including 23 non-redundant TCP genes were identified in the database of alfalfa genome (C.V XinJiangDaYe), they were classified into class I PCF (37 members) and class II: CIN (28 members) and CYC/TB1 (9 members). Their distribution on chromosome were unequally. MsTCPs belonging to PCF were expressed specifically in different organs without regularity, which belonging to CIN class were mainly expressed in mature leaves. MsTCPs belongs to CYC/TB1 clade had the highest expression level at meristem. Cis-elements in the promoter of MsTCPs were also predicted, the results indicated that most of the MsTCPs will be induced by phytohormone and stress treatments, especially by ABA-related stimulus including salinity stress. We found 20 out of 23 MsTCPs were up-regulated in 200 mM NaCl treatment, and MsTCP3/14/15/18 were significantly induced by 10 μM KCl, a K+ deficiency treatment. Fourteen non-redundant MsTCPs contained miR319 target site, 11 of them were upregulated in MIM319 transgenic alfalfa, and among them four (MsTCP3/4/10A/B) genes were directly degraded by miR319. MIM319 transgene alfalfa plants showed a salt sensitive phenotype, which caused by a lower content of potassium in alfalfa at least partly. The expression of potassium transported related genes showed significantly higher expression in MIM319 plants. ConclusionsWe systematically analyzes the MsTCP gene family at a genome-wide level and reported that miR319-TCPs model played a function in K+ up-taking and/ or transportation especially in salt stress. The study provide valuable information for future study of TCP genes in alfalfa and supplies candidate genes for salt-tolerance alfalfa molecular-assisted breeding.

Halogenated class of oximes as a new class of monoamine oxidase-B inhibitors for the treatment of Parkinson’s disease: Synthesis, biochemistry, and molecular dynamics study

Oximes are the promising structural scaffold for inhibiting monoamine oxidase (MAO)-B. Eight chalcone-based oxime derivatives were synthesized by microwave-assisted technique, and their ability to inhibit human MAO (hMAO) enzymes were tested. All compounds showed higher inhibitory activity of hMAO-B than hMAO-A. In the CHBO subseries, CHBO4 most potently inhibited hMAO-B with an IC50 value of 0.031 μM, followed by CHBO3 (IC50 = 0.075 μM). In the CHFO subseries, CHFO4 showed the highest inhibition of hMAO-B with an IC50 value of 0.147 μM. Compound CHBO4 had the highest selectivity index (SI) value of 1290.3. However, CHBO3 and CHFO4 showed relatively low SI values of 27.7 and 19.2, respectively. The -Br substituent in the CHBO subseries at the para-position in the B-ring showed higher hMAO-B inhibition than the -F substituent in the CHFO subseries. In both series, hMAO-B inhibition increased with the substituents at para-position in A-ring (-F > -Br > -Cl > -H in order). Compound CHBO4 (-F in A-ring and -Br in B-ring) was 12.6-times potent than the substituents-reversed compound CHFO3 (-Br in A-ring and -F in B-ring; IC50 = 0.391 μM). In the kinetic study, Ki values of CHBO4 and CHFO4 for hMAO-B were 0.010 ± 0.005 and 0.040 ± 0.007 μM, respectively, with competitive inhibitions. Reversibility experiments showed that CHBO4 and CHFO4 were reversible hMAO-B inhibitors. In the cytotoxicity test using the Vero cells by the MTT technique, CHBO4 had low toxicity with an IC50 value of 128.8 µg/mL. In H2O2-induced cells, CHBO4 significantly reduced cell damage by scavenging reactive oxygen species (ROS). Molecular docking and dynamics showed the stable binding mode of the lead molecule CHBO4 on the active site of hMAO-B. These results suggest that CHBO4 is a potent reversible, competitive, and selective hMAO-B inhibitor and can be used as a treatment agent for neurological disorders.

Hydrogen-rich water reduces cell damage by reducing excessive autophagy in mouse neuronal cells after oxygen glucose deprivation/reoxygenation

To investigate whether hydrogen-rich water exerts a protective effect against cellular injury by affecting the level of autophagy after oxygen glucose deprivation/reoxygenation (OGD/R) in a mouse hippocampal neuronal cell line (HT22 cells). HT22 cells in logarithmic growth phase were cultured in vitro. Cell viability was detected by cell counting kit-8 (CCK-8) assay to find the optimal concentration of Na2S2O4. HT22 cells were divided into control group (NC group), OGD/R group (sugar-free medium+10 mmol/L Na2S2O4 treated for 90 minutes and then changed to normal medium for 4 hours) and hydrogen-rich water treatment group (HW group, sugar-free medium+10 mmol/L Na2S2O4 treated for 90 minutes and then changed to medium containing hydrogen-rich water for 4 hours). The morphology of HT22 cells was observed by inverted microscopy; cell activity was detected by CCK-8 method; cell ultrastructure was observed by transmission electron microscopy; the expression of microtubule-associated protein 1 light chain 3 (LC3) and Beclin-1 was detected by immunofluorescence; the protein expression of LC3II/I and Beclin-1, markers of cellular autophagy, was detected by Western blotting. Inverted microscopy showed that compared with the NC group, the OGD/R group had poor cell status, swollen cytosol, visible cell lysis fragments and significantly lower cell activity [(49.1±2.7)% vs. (100.0±9.7)%, P < 0.01]; compared with the OGD/R group, the HW group had improved cell status and remarkably higher cell activity [(63.3±1.8)% vs. (49.1±2.7)%, P < 0.01]. Transmission electron microscopy showed that the neuronal nuclear membrane of cells in the OGD/R group was lysed and a higher number of autophagic lysosomes were visible compared with the NC group; compared with the OGD/R group, the neuronal damage of cells in the HW group was reduced and the number of autophagic lysosomes was notably decreased. The results of immunofluorescence assay showed that the expressions of LC3 and Beclin-1 were outstandingly enhanced in the OGD/R group compared with the NC group, and the expressions of LC3 and Beclin-1 were markedly weakened in the HW group compared with the OGD/R group. Western blotting assay showed that the expressions were prominently higher in both LC3II/I and Beclin-1 in the OGD/R group compared with the NC group (LC3II/I: 1.44±0.05 vs. 0.37±0.03, Beclin-1/β-actin: 1.00±0.02 vs. 0.64±0.01, both P < 0.01); compared with the OGD/R group, the protein expression of both LC3II/I and Beclin-1 in the HW group cells were notably lower (LC3II/I: 0.54±0.02 vs. 1.44±0.05, Beclin-1/β-actin: 0.83±0.07 vs. 1.00±0.02, both P < 0.01). Hydrogen-rich water has a significant protective effect on OGD/R-causing HT22 cell injury, and the mechanism may be related to the inhibition of autophagy.

Effect of mangosteen skin ethanol extract on streptozotocin-induced TNF-α expression

Introduction. Diabetes Mellitus (DM) is a significant health problem worldwide. DM with poor control of blood glucose levels can eventually cause pancreatic cell disorders, including a decrease in cell mass and function. Mangosteen rind contains xanthone compounds that can be used to protect and reduce cell damage, especially those caused by free radicals. This study aimed to analyze the administration of mangosteen peel ethanol extract on the expression of TNF-α induced by streptozotocin. Materials and Methods. The research was carried out in an experimental laboratory. The research design used was Randomized Post Test Only Control Group Design. The sample is a male rat Wistar strain. Rats were grouped into five groups, namely negative control group, positive control STZ, mangosteen peel extract at a dose of 200 mg/kg BW (K2), a dose of 400 mg/kg BW (K3), an amount of 600 mg/kg BW (K4). Administration of therapy for 14 days orally. Results. The effects of the mangosteen rind extract had a lower TNF- positive cell count of 3.83 compared to the group that was not treated with the mangosteen rind extract 19.33. All treatment groups showed a significant difference (P&lt;0.001) in the number of TNF- protein-expressing cells. This research can inform the public that mangosteen peel’s benefits can be developed as prevention and alternative treatment in humans caused by inflammation. Conclusions. This research affects the administration of ethanol extract of mangosteen peel to decrease the number of TNFpositive cells with an effective dose of 600 mg/kg BW.

Co-encapsulation of probiotics with acylglycerols in gelatin-gum arabic complex coacervates: Stability evaluation under adverse conditions

Co-encapsulation of acylglycerols and probiotics may improve the resistance of probiotics to adverse conditions. In this study, three probiotic microcapsule models were constructed using gelatin (GE)-gum arabic (GA) complex coacervate as wall material: microcapsules containing only probiotics (GE-GA), microcapsules containing triacylglycerol (TAG) oil and probiotics (GE-T-GA) and microcapsules containing diacylglycerol (DAG) oil and probiotics (GE-D-GA). The protective effects of three microcapsules on probiotic cells under environmental stresses (freeze-drying, heat treatment, simulated digestive fluid and storage) were evaluated. The results of cell membrane fatty acid composition and Fourier transform infrared (FTIR) spectroscopy revealed that GE-D-GA could improve the fluidity of cell membrane, maintain the stability of protein and nucleic acid structure, and decrease the damage of cell membrane. These characteristics supported the high freeze-dried survival rate (96.24 %) of GE-D-GA. Furthermore, regardless of thermotolerance or storage, GE-D-GA showed the best cell viability retention. More importantly, GE-D-GA provided the best protection for probiotics under simulated gastrointestinal conditions, as the presence of DAG reduced cell damage during freeze-drying and the degree of contact between probiotics and digestive fluids. Therefore, co-microencapsulation of DAG oil and probiotics is a promising strategy to resist adverse conditions.

Machine learning boosts three-dimensional bioprinting.

Three-dimensional (3D) bioprinting is a computer-controlled technology that combines biological factors and bioinks to print an accurate 3D structure in a layer- by-layer fashion. 3D bioprinting is a new tissue engineering technology based on rapid prototyping and additive manufacturing technology, combined with various disciplines. In addition to the problems in in vitro culture process, the bioprinting procedure is also afflicted with a few issues: (1) difficulty in looking for the appropriate bioink to match the printing parameters to reduce cell damage and mortality; and (2) difficulty in improving the printing accuracy in the printing process. Data- driven machine learning algorithms with powerful predictive capabilities have natural advantages in behavior prediction and new model exploration. Combining machine learning algorithms with 3D bioprinting helps to find more efficient bioinks, determine printing parameters, and detect defects in the printing process. This paper introduces several machine learning algorithms in detail, summarizes the role of machine learning in additive manufacturing applications, and reviews the research progress of the combination of 3D bioprinting and machine learning in recent years, especially the improvement of bioink generation, the optimization of printing parameter, and the detection of printing defect.

Monoclonal antibodies and amyloid removal as a therapeutic strategy for cardiac amyloidosis.

Cardiac amyloidosis (CA) is an infiltrative disease caused by progressive deposition of amyloid fibres in the heart. The most common forms include immunoglobulin light-chain and transthyretin amyloidosis. Current therapies for CA either stabilize or block the production of amyloidogenic precursors, preventing further amyloid deposition. This approach, while reducing cell damage and disease progression, does not target pre-existing amyloid deposits. Conversely, amyloid removal might stimulate functional recovery of the affected organ, thus improving quality of life and survival. A therapeutic strategy based on monoclonal antibodies capable of selectively binding amyloid deposits and inducing their removal has recently been tested in various clinical trial, with promising results, and could represent a key treatment for CA in the near future.

The natural product, echinatin, protects mice from methicillin-resistant Staphylococcus aureus pneumonia by inhibition of alpha-hemolysin expression.

Antimicrobial resistance (AMR) is a global, multifaceted crisis that poses significant challenges to the successful eradication of devastating pathogens, particularly methicillin-resistant Staphylococcus aureus (MRSA), a persistent superbug that causes devastating infections. The scarcity of new antibacterial drugs is obvious, and antivirulence strategies that reduce the pathogenicity of bacteria by weakening their virulence have become the subject of intense investigation. Alpha-hemolysin (Hla), a cytolytic pore-forming toxin, has a pivotal role in S. aureus pathogenesis. Here, we demonstrated that echinatin, a natural compound isolated from licorice, effectively inhibited the hemolytic activity of MRSA at 32 μg/mL. In addition, echinatin did not interfere with bacterial growth and had no significant cytotoxicity at the inhibitory concentration of S. aureus hemolysis. Heptamer formation tightly correlated with Hla-mediated cell invasion, whereas echinatin did not affect deoxycholic acid-induced oligomerization of Hla. Echinatin affected hemolytic activity through indirect binding to Hla as confirmed by the neutralization assay and cellular thermal shift assay (CETSA). Furthermore, qRT-PCR and western blot analyses revealed that echinatin suppressed Hla expression at both the mRNA and protein levels as well as the transcript levels of Agr quorum-sensing system-related genes. Additionally, when echinatin was added to a coculture system of A549 cells and S. aureus, it significantly reduced cell damage. Importantly, echinatin exhibited a significant therapeutic effect in an MRSA-induced mouse pneumonia model. In conclusion, the present findings demonstrated that echinatin significantly inhibits the hemolysin effect and may be a potential candidate compound for combating drug-resistant MRSA infections.

Exogenous melatonin ameliorates heat damages by regulating growth, photosynthetic efficiency and leaf ultrastructure of carnation

Carnation (Dianthus caryophyllus L.) is a floral crop that is highly valuable commercially. However, high temperatures adversely affect its growth and the quality of its cut flowers. Melatonin (MT) is a indole substance that can mitigate plant damage under heat stress. In this study, the leaves of carnation seedlings were sprayed with different concentrations of MT before exposure to high temperature. The indices of growth, physiological and chlorophyll fluorescence were measured and analyzed by the membership function method. The results showed that treatment with 100 μM MT was the most effective at ameliorating damage on carnation. We then analyzed the effects of 100 μM MT pretreatment on carnation at different time points of heat stress and found that this concentration of MT ameliorated the damage caused by heat stress, increased the content of photosynthetic pigments, enhanced the performance of photosystem II and improved photosynthesis. In addition, MT also reduced cell damage and lipid peroxidation, increased the activities of antioxidant enzymes and regulated the accumulation of osmotic substances in carnation. Moreover, MT increased the fresh/dry weight of stems and roots, promoted the opening of stomata, and protected the integrity of chloroplast structure of carnation. Compared with heat stress, pre-spraying with MT significantly down-regulated the transcription of a chlorophyll degradation gene and up-regulated the transcription of stress-related genes. Overall, this study provides a theoretical foundation for the mitigation of the adverse effects of exogenous MT under heat stress and proposes beneficial implications for the management of other plants subjected to global warming.

Algae-mediated bioremediation of ciprofloxacin through a symbiotic microalgae-bacteria consortium

The ciprofloxacin treating via microalga and its microalgae-bacteria consortium was investigated for discussing the potential application of microalgae-mediated bioremediation. As results, the maximum removal efficiency of ciprofloxacin by pure microalgae and the consortium was 87.5 ± 3.5 % (5 mg/L) and 96.1 ± 0.07 % (40 mg/L), respectively. The consortium enhanced the degradation rate to 0.81 d−1 compared with the pure microalgae (0.27 d−1). To reveal the symbiotic mechanism, extracellular polymeric substances, pigments contents, antioxidant enzymes and symbiotic bacterial community were analyzed. The malondialdehyde content in the pure microalgae (1622.6 ± 38.7 nmol/mg protein) was higher than that in the consortium (298.34 ± 2.4 nmol/mg protein), and there were obvious chlorophyll b accumulations (approximately 90 %) in consortium. In addition, the symbiotic bacteria had a positive effect on microalgal secretion of fulvic acid-type components. As mechanism, symbiotic bacteria improved ciprofloxacin biodegradation by reducing cell damage and secreting fulvic acid. The presence of Phycisphaeraceae and Rhizobiaceae, nitrogen fixation bacteria, in the consortium suggest that improvement of ciprofloxacin biodegradation might be associated with nitrogen co-metabolism as well. Collectively, this work elucidates the mechanism of enhancing elimination of ciprofloxacin via microalgae-bacteria consortium and accelerates development of microalgae-mediated aquaculture tailwater bioremediation.

Bioprinted Schwann and Mesenchymal Stem Cell Co-Cultures for Enhanced Spatial Control of Neurite Outgrowth.

Bioprinting nerve conduits supplemented with glial or stem cells is a promising approach to promote axonal regeneration in the injured nervous system. In this study, we examined the effects of different compositions of bioprinted fibrin hydrogels supplemented with Schwann cells and mesenchymal stem cells (MSCs) on cell viability, production of neurotrophic factors, and neurite outgrowth from adult sensory neurons. To reduce cell damage during bioprinting, we analyzed and optimized the shear stress magnitude and exposure time. The results demonstrated that fibrin hydrogel made from 9 mg/mL of fibrinogen and 50IE/mL of thrombin maintained the gel's highest stability and cell viability. Gene transcription levels for neurotrophic factors were significantly higher in cultures containing Schwann cells. However, the amount of the secreted neurotrophic factors was similar in all co-cultures with the different ratios of Schwann cells and MSCs. By testing various co-culture combinations, we found that the number of Schwann cells can feasibly be reduced by half and still stimulate guided neurite outgrowth in a 3D-printed fibrin matrix. This study demonstrates that bioprinting can be used to develop nerve conduits with optimized cell compositions to guide axonal regeneration.

Astragaloside IV mitigates cerebral ischaemia-reperfusion injury via inhibition of P62/Keap1/Nrf2 pathway-mediated ferroptosis

Cerebral ischaemia-reperfusion injury (CIRI) is a critical component of ischaemic stroke pathogenesis. Ferroptosis contributes to and aggravates CIRI, whereas the P62/Kelch-like ECH-associated protein 1 (Keap1)/NF-E2-related factor 2 (Nrf2) pathway exerts neuroprotective effects. Astragaloside IV (AST IV) is the primary active ingredient of Astragalus, an herb with anti-CIRI properties used in traditional Chinese medicine. However, the mechanism of its anti-CIRI action is unclear. This study examined the mechanisms underlying the anti-CIRI action of AST IV using a combination of in vitro and in vivo approaches. We established an erastin-induced ferroptosis model, oxygen and glucose deprivation/reoxygenation (OGD/R)-induced model in SH-SY5Y cells, and middle cerebral artery occlusion-reperfusion (MCAO/R) model using Sprague–Dawley rats. The extent of cell damage and brain damage in rats, ferroptosis indicator changes, and expression of P62, Keap1, and Nrf2 were investigated. AST IV inhibited erastin-induced ferroptosis, attenuated OGD/R-induced cell damage, and ameliorated sensorimotor dysfunction and injury in the MCAO/R model. Further, AST IV promoted Nrf2 activation, inhibited ferroptosis, and reduced cell damage. Notably, these effects were inhibited by ML385, an Nrf2 inhibitor. AST IV increased the P62 and Nrf2 levels and decreased the Keap1 levels. P62 silencing reduced the effects of AST IV on the P62/Keap1/Nrf2 pathway and ferroptosis. Our findings suggest that AST IV mitigates CIRI by inhibiting ferroptosis via activation of the P62/Keap1/Nrf2 pathway. This study provides an important scientific basis and direction for the application and research of AST IV and provides new potential targets and ideas for the study of the pathological mechanism of CIRI.

Berberine Alleviates the Damage, Oxidative Stress and Mitochondrial Dysfunction of PC12 Cells Induced by High Glucose by Activating the KEAP1/Nrf2/ARE Pathway.

Diabetic encephalopathy (DE) is one of the major chronic complications of diabetes mellitus. This study aims to investigate the inhibitory effect of berberine (BBR) on the damage of PC12 cells induced by high glucose (HG). Differentiated PC12 cells were treated with different concentrations of glucose/BBR. The cell morphology, cell viability, lactate dehydrogenase (LDH) activity, apoptosis, oxidative stress (OS), mitochondrial structure, mitochondrial membrane potential (MMP), mitochondrial complex I-V activity, and adenosine triphosphate (ATP) levels were evaluated. The mRNA and protein levels of the Keap1/Nrf2/ARE pathway-related genes were assessed by RT-qPCR and Western blot. High-dose BBR and HG jointly treated-PC12 cells were treated with Nrf2-specific inhibitor ML385 to further verify whether Nrf2 was the target of BBR. The results showed that BBR inhibited cell damage, OS, and mitochondrial dysfunction induced by HG. The inhibitory effect of high BBR was more significant. The Keap1/Nrf2/ARE pathway was inhibited in PC12 cells induced by HG. BBR could activate the Keap1/Nrf2/ARE pathway, thus up-regulating the expression levels of antioxidant enzymes. ML385 antagonized the ameliorating effect of BBR on OS and mitochondrial dysfunction. The conclusion is that BBR can activate the Keap1/Nrf2/ARE pathway, upregulate the expression patterns of antioxidant enzymes, and reduce cell damage, OS, and mitochondrial dysfunction of PC12 cells induced by HG.

LncRNA CRNDE binds hnRNPA1 to facilitate carbon monoxide poisoning-induced delayed encephalopathy via inhibiting UCHL5-mediated SMO deubiquitination.

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is one of the most common complications following carbon monoxide intoxication. Long noncoding RNAs (lncRNAs) exert critical functions in numerous neurological disorders. We intended to investigate the role of CRNDE in DEACMP. The DEACMP model in rats and the oxygen-glucose deprivation/reoxygenation (OGD/R) model in PC-12 cells were established. Brain and cell injuries were assessed with H&E staining, Nissl staining, TUNEL and CCK8 assays, respectively. Related proteins and RNAs were quantified with western blot and qRT-PCR. The N6-methyladenosine (m6A) level was determined using MeRIP-qPCR and immunofluorescence. Loss and gain function studies were performed to investigate the biological function of CRNDE. The potential mechanisms between each factor were explored using RNA immunoprecipitation, RNA-pull down and co-immunoprecipitation. CRNDE was increased in the hippocampal tissues of DEACMP rats and in OGD/R-treated PC-12 cells, which was positively correlated to m6A modification. Knockdown of CRNDE reduced cell damage and elevated UCHL5 and SMO expressions in OGD/R-treated PC-12 cells. hnRNPA1 was upregulated in DEACMP. In addition, inhibiting hnRNPA1 prevented apoptosis in PC-12 cells subjected to OGD/R. hnRNPA1 bound to CRNDE and remained in the nucleus, which inhibited UCHL5 expression through the formation of CRNDE-hnRNPA1-mRNA complex. UCHL5 could inhibit SMO ubiquitination and suppress PC-12 cell apoptosis during OGD/R. CRNDE silencing blocked brain injury in DEACMP, while knocking down UCHL5 reversed these effects. CRNDE interacted with hnRNPA1 to facilitate DEACMP via inhibition of UCHL5-mediated SMO deubiquitination. CRNDE might be a latent therapeutic target for treating DEACMP.

Synthesis characterisation and neuroprotectivity of Silybum marianum extract loaded chitosan nanoparticles

Aim Silybum marianum extract (SME) possesses neuroprotective potency through its high antioxidant content. We attempted to increase the effectiveness of SME by encapsulating them in chitosan. Neuroprotective potency of SME and SME-loaded chitosan nanoparticles (SME-CNPs) were shown in SH-SY5Y cell line against H2O2-induced oxidative stress. Methods We produced CNPs and SME-CNPs by ionic gelation method and properly determined their physical characteristics. Encapsulation efficiency, loading capacity, and in vitro release tests were performed for SME-CNPs. The neurotoxicity and neuroprotective efficiency in SH-SY5Y cell line against H2O2 was also investigated. Results The size of SME-CNPs was 168.2 ± 11.12 nm with zeta potential 10.6 ± 1.0 mV. The encapsulation efficiency and loading capacity were successfully achieved at 96.6% and 1.89% respectively. SME and SME-CNPs improved cell viability higher than 80%, and SME-CNPs exhibited significant neuroprotective effects against H2O2 damage. Conclusions It was concluded that SME and SME-CNPs highly prevent damage caused by H2O2 and reduce cell damage in vitro by their neuroprotective effects.

Evaluating the effectiveness of a training program to support nurses to administer cryopreserved hematopoietic stem cells by intravenous push method.

A training program was developed to prepare registered nurses (RNs) at one cellular therapy centre to administer cryopreserved cells by intravenous (IV) push method. There are two main methods of infusion for dimethyl sulfoxide (DMSO) cryopreserved hematopoietic stem cell (HSC) products, gravity drip and IV push. Administering DMSO by either route can cause hypersensitivity reactions. Administration of HSCs by gravity drip is slower, resulting in fewer DMSO reactions. However, prolonged exposure of DMSO once the cells are thawed increases the risk of cellular damage. The faster IV push method reduces cell damage and decreases staff time. An environmental review within Canadian transplant centres found that in most adult centres, nurses administer by gravity drip, and when IV push is required, cryopreserved hematopoietic stem cells are administered by physicians. Our centre's method was IV push by a physician or nurse practitioner (NP). As transplant numbers grew, capacity to perform this skill needed to expand. To maintain the current benefits of the IV push method and increase capacity in a hematopoietic transplant program, the role of infusing stem cells by the IV push method was transitioned from the NPs and physicians to RNs. A successful training program utilizing simulation to support these oncology nurses in learning the new skill was developed and evaluated.

PENGARUH PEMBERIAN EKSTRAK ISOFLAVON TEMPE TERHADAP TINGKAT STRESS OKSIDATIF PADA TIKUS PUTIH JANTAN GALUR WISTAR (Rattus novergicus) SETELAH DIINDUKSI DENGAN DOSIS TOKSIK PARASETAMOL

ABSTRACT&#x0D; Background: As a producing country and at the same time the largest consumer of tempeh in the world, Indonesia has become the largest soybean market in Asia. As much as 50% of soybean consumption in Indonesia is done in the form of tempeh. Tempe is a potential food ingredient as a hepatoprotector. The content of isoflavones in tempeh has been shown to protect rat liver function under stress conditions. Isoflavones contained in tempeh have activity as antioxidants, which can prevent oxidation reactions from occurring by working as reducing agents and protecting cell membranes from oxidation, as well as counteracting free radicals by stopping chain reactions and protecting cells from DNA activation so as to reduce cell damage. This situation has prompted the authors to investigate the effect of the isoflavone extract of tempeh on the histochemistry and histopathology of the livers of male white Wistar rats (Rattus novergicus) after being induced by toxic doses of Paracetamol.&#x0D; Methods: This study was an experimental study using the Randomized Posttest Only Control Group Design to determine the level of oxidative stress after administration of tempeh isoflavone extract to male white rats (Rattus novergicus) induced with a toxic dose of paracetamol. 5 groups, namely group 1 was given tempe extract 160 mg/kgBB, group 2 was given tempe extract 320 mg/kgBB, group 3 was given tempe extract 640 mg/kgBB, group 5 was given distilled water and group 6 was given 1% NaCMC solution. Each rat was treated for 14 days. On day 12, 13 and 14 rats were given paracetamol at a dose of 900 mg/kg BW in 1% NaCMC. And on the 15th day, rat blood serum was examined for levels of SGOT, SGPT and MDA.&#x0D; Results: It was found that tempeh at a dose of 640 mg/kgBW could significantly reduce SGOT, SGPT and MDA levels (p&lt;0.05) compared to other doses as well as distilled water and 1% NaCMC.&#x0D; Conclusion: So it can be concluded that tempeh can be an alternative source of antioxidants that can protect liver cells from the effects of substances that can damage the liver.&#x0D; Keywords: Tempe, SGOT, SGPT, MDA

Storage Quality Variation of Mushrooms (Flammulina velutipes) after Cold Plasma Treatment.

Flammulina velutipes is susceptible to mechanical damage, water loss, microbial growth, and other factors that lead to postharvest deterioration, thereby shortening the storage period. The purpose of this study was to analyze the effects of cold plasma treatment on the physicochemical properties and antioxidant capacity of F. velutipes during storage at 4 °C for 21 days. Compared to the control group, cold plasma cold sterilization (CPCS) treatment (150 Hz, 95 kV for 150 s) effectively inhibited the growth and multiplication of microorganisms on the surface of F. velutipes, with no significant effect on the fresh weight change and the superoxide anion generation rate, but with a higher postharvest 1,1-dephenyl-2-picrylhydrzyl (DPPH) clearance rate. Moreover, CPCS increased antioxidant enzyme activities, delayed both malondialdehyde (MDA) accumulation and vitamin C loss, inhibited the browning reaction and polyphenol oxidases (PPO) activity and protected F. velutipes cell membrane from disruption. In general, CPCS not only achieved bacteriostatic effects on F. velutipes during storage, but also reduced cell damage from free radical oxidation, resulting in better postharvest quality and longer shelf life.

Grafting promoted antioxidant capacity and carbon and nitrogen metabolism of bitter gourd seedlings under heat stress.

Heat stress can limit vegetable growth, and this can lead to constraints on agricultural production. Grafting technologies, however, can be used to alleviate various plant stresses. In this study, the differences in the heat stress impacts and recovery abilities of pumpkin and luffa rootstocks for bitter gourd were analyzed in terms of their antioxidant activity and carbon and nitrogen metabolism. Compared with the un-grafted and self-grafted bitter gourd, which suffered from heat stress at 40°C for 24h, heterologously grafted bitter gourd showed higher heat stability of the cell membrane (relative conductivity and malondialdehyde content were reduced), reduced oxidative stress (antioxidant enzyme activity was increased and the reactive oxygen species content reduced), and increased enzyme activity (sucrose phosphate synthase, sucrose synthase, neutral invertase, and acid invertase) and sugar content (soluble sugar, sucrose, fructose, and glucose) in carbon metabolism. The enzyme activity (nitrate reductase, nitrite reductase, and glutamine synthetase) and product content (nitrate and nitrite) of nitrogen metabolism were also found to be increased, and this inhibited the accumulation of ammonium ions. After the seedlings were placed at 25°C for 24h, the heterogeneous rootstocks could rapidly restore the growth of the bitter gourd seedlings by promoting the antioxidant and carbon and nitrogen metabolism systems. When luffa was used as rootstock, its performance on the indexes was better than that of pumpkin. The correlation between the various indicators was demonstrated using a principal component and correlation analysis. The luffa rootstock was found to be more conducive to reducing cell damage and energy loss in bitter gourd seedlings caused by heat induction through the maintenance of intracellular redox homeostasis and the promotion of carbon and nitrogen metabolism.