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β-aminoisobutyric acid accelerates the proliferation and differentiation of MC3T3-E1 cells via moderate activation of ROS signaling.

Osteoporosis is one of the bone-metabolic diseases associated with decreased bone renewal and bone mineral density. β-aminoisobutyric acid (BAIBA), a natural thymine catabolite, can reduce inflammation in skeletal muscle and alleviate hepatic endoplasmic reticulum stress. However, the roles of BAIBA in osteoblast proliferation and differentiation remain largely unknown.

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Biochemical Measurement of Glycogen: Method to Investigate the AMPK-Glycogen Relationship.

Glycogen is a main carbohydrate energy storage primarily found in fungi and animals. It is a glucose polymer that comprises α(1-4) glycosidic linkages attaching UDP-glucose molecules linearly and α(1-6) linkages branching glucose chains every 8-10 molecules to the main backbone chain. Glycogen synthase, branching enzyme, and glycogen phosphorylase are key enzymes involved in glycogen synthesis and degradation. These enzymes are tightly regulated by upstream kinases and phosphatases that respond to hormonal cues in order to coordinate storage and degradation and meet the cellular and organismal metabolic needs. The 5'AMP-activated protein kinase (AMPK) is one of the main regulators of glycogen metabolism. Despite extensive research, the role of AMPK in glycogen synthesis and degradation remains controversial. Specifically, the level and duration of AMPK activity highly influence the outcome on glycogen reserves. Here, we describe a rapid and robust protocol to efficiently measure the levels of glycogen in vitro. We use the commercially available glycogen determination kit to hydrolyze glycogen into glucose, which is oxidized to form D-gluconic acid and hydrogen peroxide that react with the OxiRed/Amplex Red probe generating a product that could be detected either in a colorimetric or fluorimetric plate format. This method is quantitative and could be used to address the role of AMPK in glycogen metabolism in cells and tissues. Summary This chapter provides a quick and reliable biochemical quantitative method to measure glycogen in cells and tissues. Briefly, this method is based on the degradation of glycogen to glucose, which is then specifically oxidized to generate a product that reacts with the OxiRed probe with maximum absorbance at 570 nm. This method is very accurate and highly sensitive. In the notes of this chapter, we shed the light on important actions that should be followed to get reliable results. We also state advantages and disadvantages of this method in comparison to other glycogen measurement techniques.

2969 related Products with: Biochemical Measurement of Glycogen: Method to Investigate the AMPK-Glycogen Relationship.

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Two sesquiterpene aminoquinones protect against oxidative injury in HaCaT keratinocytes via activation of AMPKα/ERK-Nrf2/ARE/HO-1 signaling.

To investigate the cytoprotective effects of two sesquiterpene aminoquinones isolated from the marine sponge Dysidea fragilis, Dysidaminone H (DA8) and 3'-methylamino-avarone (DA14), we examined their effects against hydrogen peroxide (HO)-induced oxidative injury in human keratinocyte cell line and elucidated the underlying mechanisms.

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Carboxymethylated chitosan protects Schwann cells against hydrogen peroxide-induced apoptosis by inhibiting oxidative stress and mitochondria dependent pathway.

Carboxymethylated chitosan (CMCS) has many beneficial effects, including anti-oxidant and anti-apoptotic actions. However, the mechanisms by which CMCS protect against oxidative stress induced damage to Schwann cells (SCs) remains unclear. The present study aimed to investigate the mechanism by which CMCS protects SCs against hydrogen peroxide (HO) induced damage. HO was used to establish a model of oxidative stress injury in SCs to mimic the development of nerve injury in vitro. Different concentrations (50, 100 and 200 µg/ml) of CMCS were added to test whether CMCS was capable of protecting SCs from HO induced damage. MTT, LDH release and Annexin V/FITC assays were then performed. Levels of reactive oxygen species were detected using a reactive oxygen species assay kit, the mitochondrial membrane potential (ΔΨm) of SCs was analyzed by rhodamine123 fluorescence staining, the synthesis of Bcl-2, Bax, cytochrome c and caspase-3 were analyzed by real-time PCR and Western blot analysis. The results showed that CMCS protected SCs from apoptosis, decreased LDH release and enhanced cell viability, also decreased reactive oxygen species levels and increased ΔΨm. Additional experiments demonstrated that CMCS could decrease protein expression of Bax, cytochrome c and caspase-3, while promote Bcl-2 protein expression induced by HO. Taken together, the finding of this study indicated that CMCS prevented HO-induced damage to SCs through the mitochondrial dependent pathway.

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Bone marrow mesenchymal stem cell-derived exosomal miR-21 protects C-kit+ cardiac stem cells from oxidative injury through the PTEN/PI3K/Akt axis.

Stem cell (SC) therapy for ischemic cardiomyopathy is hampered by poor survival of the implanted cells. Recently, SC-derived exosomes have been shown to facilitate cell proliferation and survival by transporting various proteins and non-coding RNAs (such as microRNAs and lncRNAs). In this study, miR-21 was highly enriched in exosomes derived from bone marrow mesenchymal stem cells (MSCs). Interestingly, exosomes collected from hydrogen peroxide (H2O2)-treated MSCs (H-Exo) contained higher levels of miR-21 than exosomes released from MSCs under normal conditions (N-Exo). The pre-treatment of C-kit+ cardiac stem cells (CSCs) with H-Exos resulted in significantly increased levels of miR-21 and phosphor-Akt (pAkt) and decreased levels of PTEN, which is a known target of miR-21. AnnexinV-FITC/PI analysis further demonstrated that the degree of oxidative stress-induced apoptosis was markedly lower in H-Exo-treated C-kit+ CSCs than that in N-Exo-treated cells. These protective effects could be blocked by both a miR-21 inhibitor and the PI3K/Akt inhibitor LY294002. Therefore, exosomal miR-21 derived from H2O2-treated MSCs could be transported to C-kit+ cardiac stem cells to functionally inhibit PTEN expression, thereby activating PI3K/AKT signaling and leading to protection against oxidative stress-triggered cell death. Thus, exosomes derived from MSCs could be used as a new therapeutic vehicle to facilitate C-kit+ CSC therapies in the ischemic myocardium.

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Fluorescence ELISA based on glucose oxidase-mediated fluorescence quenching of quantum dots for highly sensitive detection of Hepatitis B.

Herein, we present a novel sandwich fluorescence enzyme linked immunosorbent assay (ELISA) for highly sensitive detection of Hepatitis B virus surface antigen (HBsAg) based on glucose oxidase (GOx)-induced fluorescence quenching of mercaptopropionic acid-modified CdTe quantum dots (MPA-QDs). In this system, hydrogen peroxide (HO) sensitive MPA-QDs was used as a signal output, and glucose oxidase (GOx) was used as label which can generate HO via catalytic oxidation of glucose. The proposed method showed dynamic linear detection of HBsAg both in the range of 47pgmL ~ 380pgmL and 0.75ngmL ~ 12.12ngmL. The detection limit of the proposed fluorescence ELISA was 1.16pgmL, which was approximately 430-fold lower than that of horseradish peroxidase (HRP)-based conventional ELISA. The average recoveries for HBsAg-spiked serum samples ranged from 98.0% to 126.8% with the relative standard derivation below 10%, thus indicating acceptable precision and high reproducibility of the proposed fluorescence ELISA for HBsAg detection. Additionally, the developed method showed no false positive results analyzing 35 real HBsAg-negative serum samples, and exhibited excellent agreement (R=0.9907) with a commercial time-resolved fluorescence immunoassay (TRFIA) kit for detecting 31 HBsAg-positive serum samples. In summary, the proposed method based on fluorescence quenching of HO sensitive QDs is considerably to be an excellent biodetection platform with ultrahigh sensitivity, good accuracy and excellent reliability.

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Efficient synthesis and first regioselective C-6 direct arylation of imidazo[2,1-c][1,2,4]triazine scaffold and their evaluation in HO-induced oxidative stress.

Oxidative stress and apoptosis are both associated with various acute and chronic disorders. Thus, the aim of the present study is to synthesize imidazo[2,1-c][1,2,4]triazines derivatives and to evaluate their effects in HO-induced oxidative stress in human neuroblastoma cell line (SH-SY5Y cells). The effects of the compounds on cell viability were measured by MTT assay and the changes in stress and apoptosis-related proteins were investigated by PathScan Stress and Apoptosis Signaling Antibody Array kit and Western Blot technique. In particular, four compounds were found to protect SH-SY5Y cells from HO-induced toxicity by increasing Bcl-2/Bax ratio, regulating PI3-K/Akt cascade and inhibiting the ERK pathway.

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[Antioxidant effects of celastrol against hydrogen peroxide-induced oxidative stress in the cell model of amyotrophic lateral sclerosis].

To investigate the anti-oxidative effect of celastrol on HO-induced oxidative stress in the cell model of amyotrophic lateral sclerosis (ALS) and its molecular mechanism, NSC34 motor neuron-like cells were transfected with EGFP-G93A-SOD1 plasmid and used as in vitro ALS cell model. SOD1 transfected NSC34 cells were treated with different doses of HO and celastrol. The survival rate of the cells was detected by CCK-8 assay, and malondialdehyde (MDA) content was detected by corresponding kit. The mRNA expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione S-transferases (GST) were detected by real-time PCR. The activation of intracellular MEK/ERK and PI3K/Akt signal pathways was detected by Western blot. The results showed that pre-incubation of celastrol (50 nmol/L) for 4 h prior to HO (10 μmol/L) co-treatment for another 24 h significantly attenuated HO-induced cell death and MDA level in SOD1 transfected NSC34 cells. Real-time PCR showed that the mRNA expressions of GCLC and GST were enhanced with pre-incubation of celastrol. Celastrol quickly induced phosphorylation of ERK1/2 and Akt within 30 min and 1 h respectively in SOD1 transfected NSC34 cells. Pharmacological inhibitors of MEK (PD98059, 10 μmol/L) or Akt (MK2206, 10 μmol/L) could reverse the phosphorylation of ERK1/2 and Akt, and abolish up-regulation of GCLC and GST induced by celastrol at mRNA levels. Taken together, we conclude that celastrol exerts a beneficial antioxidant effect in SOD1NSC34 cells, which might be dependent on MEK/ERK and PI3K/Akt signaling pathway activation.

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Increased MMAB level in mitochondria as a novel biomarker of hepatotoxicity induced by Efavirenz.

Efavirenz (EFV), a non-nucleoside reverse transcriptase inhibitor (NNRTI), has been widely used in the therapy of human immunodeficiency virus (HIV) infection. Some of its toxic effects on hepatic cells have been reported to display features of mitochondrial dysfunction through bioenergetic stress and autophagy, etc. However, alteration of protein levels, especially mitochondrial protein levels, in hepatic cells during treatment of EFV has not been fully investigated.

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[Effect and related mechanism of miRNA-21 on hydrogen peroxide-induced C-kit(+) cardiac stem cells apoptosis].

To explored the effect and related mechanism of miRNA-21 on hydrogen peroxide-induced C-kit(+) cardiac stem cells apoptosis. C-kit(+) cardiac stem cells were isolated from SD rats by the methods of enzyme digestion and magnetic bead. Cells were divided into the following experimental groups: (1) negative control mimics (NCM)group: cells were transfected with negative control miRNA-21 mimics for 48 hours; (2)mimics group: cells were transfected with miRNA-21 mimics for 48 hours; (3) NCM+ H(2)O(2) group: negative control miRNA-21 mimics were transfected into cells for 48 hours and then treated with 100 μmol H(2)O(2) for 2 hours; (4)mimics+ H(2)O(2) group: miRNA-21 mimics were transfected into cells for 48 hours and then treated with 100 μmol H(2)O(2) for 2 hours. mRNA of miRNA-21 was detected by RT-PCR. The apoptosis rate of C-kit(+) cardiac stem cells was determined using the annexin V-FITC/PI staining assay. Western blot was employed to measure the expression of apoptosis related proteins(Caspase-3, Bax, and Bcl-2). (1) Compared with the NCM group, the mRNA expression level of miRNA-21 was significantly up-regulated in mimics group, while obviously down-regulated in NCM+ H(2)O(2) group(all <0.05). Compared with the mimics group, the mRNA expression levels of miRNA-21 in mimics+ H(2)O(2) group was significantly downregulated (<0.05), but remarkably upregulated compared with the NCM+ H(2)O(2) group(<0.05). (2) Flow cytometry results indicated that the early apoptosis rates were similar between the NCM group and mimics group ((4.57±3.45)% vs. (5.13±3.21)%, >0.05). Compared with the NCM group, the early apoptosis rates were remarkably increased ((79.07±5.75)% vs.(4.57±3.45)%, <0.05) in NCM+ H(2)O(2) group. Compared with the mimics group, the early apoptosis was significantly up-regulated in the mimics+ H(2)O(2) group ((30.27±1.36)% vs.(5.13±3.21)%, <0.05), which were further down-regulated in mimics+ H(2)O(2) group compared with the NCM+ H(2)O(2) group ((30.27±1.36)% vs.(79.07±5.75)%, <0.05). (3) Western blot results showed similar protein expression of Caspase-3, Bax and Bcl-2 between NCM group and mimics group(all >0.05). Compared with the NCM group, the Caspase-3 and Bax protein expression was significantly increased in NCM+ H(2)O(2) group (all <0.05), but the protein expression level of Bcl-2 was similar between the 2 groups(>0.05). The Caspase-3 and Bax protein expression was markedly decreased, while Bcl-2 apparently increased in the mimics+ H(2)O(2) group compared with the NCM+ H(2)O(2) group(all <0.05). Overexpression of miRNA-21 protects the C-kit(+) cardiac stem cells from apoptosis caused by oxidative stress through downregulating proapoptotic and upregulating the antiapoptotic proteins.

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