scholarly journals Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

2020 ◽  
Author(s):  
Yajing Wang ◽  
Bingxian Liu ◽  
Qingyue Han ◽  
Khalid Mehmood ◽  
Fazul Nabi ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Beclin 1 ◽  
Protective Effects ◽  
Human Beings ◽  
Caspase 9 ◽  
Nano Material ◽  
Cyt C ◽  
Hepatocyte Damage

Abstract Background: Fluorine is widespread in the environment, and the injurious impacts of fluoride underscore its significance for public health. The long-term presence of fluorine in environment could be a risk in hepatotoxicity for both human beings and animals. Important role of selenium in mitigation of heavy metal toxicity via regulating autophagy and apoptosis is well-known. Further, nano-Se is a common artificial nano material, with higher biological activity and lower toxicity. The aim of the current study was to examine whether nano-Se supplementation can reduce the effects of fluoride-induced hepatocytes autophagy and apoptosis. Results: Here, we report that fluoride exposure induces apoptosis and autophagy with nucleus broken, dissolved and disappeared of hepatocyte, contributing to its hepatotoxicity. More importantly, Cyt-C and Beclin-1/Bcl-2 pathways are involved in the regulation of autophagy and apoptosis via targeting Caspase-9, Caspase-3, P53, Bax, LC3, ATG-5, P62 and mTOR expressions. Conclusion: Nano-Se is capable to alleviate fluoride-induced hepatocyte damage, that selenium can be prefer to prevent chronic fluorosis-induced autophagy and apoptosis by regulating Cyt-C and Beclin-1/Bcl-2 signaling pathway. In precisely, NaF-induced the liver injury by activating autophagy and apoptosis, which indicate that fluorine exposure, pose an ecological risk to human beings and animals. Nano-Se has protective effects against fluoride-induced hepatocytes.

Protective efficacy of carnosic acid against hydrogen peroxide induced oxidative injury in HepG2 cells through the SIRT1 pathway

2015 ◽  
Vol 93 (8) ◽  
pp. 625-631 ◽  
Author(s):  
Yan Hu ◽  
Ning Zhang ◽  
Qing Fan ◽  
Musen Lin ◽  
Ce Zhang ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Hepg2 Cells ◽  
Manganese Superoxide Dismutase ◽  
Caspase 3 ◽  
Protective Efficacy ◽  
B Cell Lymphoma ◽  
Sirtuin 1 ◽  
Carnosic Acid ◽  
Protective Effects ◽  
Hepatocyte Damage

Carnosic acid (CA), found in rosemary, has been reported to have antioxidant and antiadipogenic properties. Here, we investigate the molecular mechanism by which CA inhibits hydrogen peroxide (H2O2)-induced injury in HepG2 cells. Cells were pretreated with 2.5–10 μmol/L CA for 2 h and then exposed to 3 mmol/L H2O2 for an additional 4 h. CA dose-dependently increased cell viability and decreased lactate dehydrogenase activities. Pretreatment with CA completely attenuated the inhibited expression of manganese superoxide dismutase (MnSOD) and the B-cell lymphoma-extra large (Bcl-xL), and reduced glutathione activity caused by H2O2, whereas it reversed reactive oxygen species accumulation and the increase in cleaved caspase-3. Importantly, sirtuin 1 (SIRT1), a NAD+-dependent deacetylase, was significantly increased by CA. Considering the above results, we hypothesized that SIRT1 may play important roles in the protective effects of CA in injury induced by H2O2. As expected, SIRT1 suppression by Ex527 (6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide) and siRNA-mediated SIRT1 silencing (si-SIRT1) significantly aggravated the H2O2-induced increased level of cleaved caspase-3 but greatly reduced the decreased expression of MnSOD and Bcl-xL. Furthermore, the positive regulatory effect of CA was inhibited by si-SIRT1. Collectively, the present study indicated that CA can alleviate H2O2-induced hepatocyte damage through the SIRT1 pathway.

scholarly journals An Essential Role of Polymeric Adhesives in the Reinforcement of Acidified Paper Relics

Polymers ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 207
Author(s):  
Jiaojiao Liu ◽  
Huiping Xing ◽  
Yajun Zhou ◽  
Xiaolian Chao ◽  
Yuhu Li ◽  
...  
Keyword(s):  
Essential Role ◽  
Polyvinyl Butyral ◽  
Scientific Basis ◽  
Water Soluble ◽  
Wheat Starch ◽  
Protective Effects ◽  
Ft Ir ◽  
Starch Paste

Paper acidification causes paper relics to undergo embrittlement and decay, to form dregs, and even to break upon a single touch; therefore, reinforcement and deacidification treatments are essential steps for paper conservation and to retard the deterioration and prolong the life of objects. Polymeric adhesives play an essential role in reinforcement and deacidification treatments, although it is not well studied. In this work, the effect of polymeric adhesives on the conservation process and their protective effects on acidified paper relics were studied. Firstly, three polymeric adhesives, including wheat starch paste, polyvinyl butyral (PVB), and polyvinyl alcohol (PVA), were selected as research objects. Subsequently, their effects on four popular conservation methods were further discussed, including traditional mounting, hot-melt with silk net, alcohol-soluble cotton mesh, and water-soluble cotton mesh. Additionally, as an example, the reversibility and long-term durability of water-soluble adhesive PVA-217 were assessed. Using a computer measured and controlled folding endurance tester, pendulum tensile strength tester, tear tester, burst tester, FT-IR, video optical contact angle tester, and other instruments, the conservation application of water-soluble adhesives in paper relics was evaluated. This study provides a scientific basis and experimental data for the application of polymeric adhesives in the conservation of paper relics.

scholarly journals Guaiane-Type Sesquiterpenoids From Dendranthema morifolium (Ramat.) S. Kitam Flowers Protect H9c2 Cardiomyocyte From LPS-Induced Injury

2019 ◽  
Vol 14 (7) ◽  
pp. 1934578X1986417
Author(s):  
Beibei Zhang ◽  
Mengnan Zeng ◽  
Meng Li ◽  
Wenjing Chen ◽  
Benke Li ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Creatine Phosphate ◽  
Cardiomyocyte Apoptosis ◽  
Exocyclic Double Bond ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Caspase 9 ◽  
Necrosis Factor Alpha ◽  
Thiazolyl Blue Tetrazolium Bromide ◽  
Tnf Α

This study investigated the protective effects of guaiane-type sesquiterpenoids isolated from Dendranthema morifolium (Ramat.) S. Kitam flowers on lipopolysaccharide (LPS)-induced injury in H9c2 cardiomyocyte. Cell viability was determined by thiazolyl blue tetrazolium bromide (MTT). The content of released tumor necrosis factor alpha (TNF- α) and interleukin 6 (IL-6) was evaluated by enzyme-linked immunosorbent assay. The levels of lactate dehydrogenase (LDH) and creatine phosphate kinase (CK) were measured by using commercial available kits. The protein expression levels of pelF2 α, GRP78, Bax, caspase-3, caspase-9, Bcl-2, LC3-II, and p62 were measured by in-cell Western. Flow cytometry was used to detect H9c2 cardiomyocyte apoptosis. Compounds 5, 7, 1, 8, and 2 exhibited the effects of cardioprotection and activity sequence enhancement. The levels of IL-6, TNF- α, LDH, CK, pelF2 α, GRP78, Bax, caspase-3, caspase-9, p62, and H9c2 cardiomyocyte apoptosis were increased in LPS-treated H9c2 cardiomyocyte, while those of Bcl-2 and LC3-II were decreased. These effects could be effectively reversed by compounds 5, 7, 1, 8, and 2. Results demonstrated that the guaiane-type sesquiterpenoids could prevent LPS-induced injury in cardiomyocyte by decreasing endoplasmic reticulum (ER) stress, apoptosis, and autophagy as well as downregulating the inflammatory mediators. In addition, the active groups of guaiane-type sesquiterpenoids might be the angelate at C-8 and the exocyclic double bond at C-11.

scholarly journals Mechanism of Heshouwuyin inhibiting the Cyt c/Apaf-1/Caspase-9/Caspase-3 pathway in spermatogenic cell apoptosis

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Hongjie Wang ◽  
Juan Zhu ◽  
Liping Jiang ◽  
Boying Shan ◽  
Peihan Xiao ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Caspase 3 ◽  
Spermatogenic Cell ◽  
Caspase 9 ◽  
Cyt C

Propofol Attenuates Peroxynitrite-mediated DNA Damage and Apoptosis in Cultured Astrocytes

2004 ◽  
Vol 101 (6) ◽  
pp. 1363-1371 ◽  
Author(s):  
Rosaria Acquaviva ◽  
Agata Campisi ◽  
Paolo Murabito ◽  
Giuseppina Raciti ◽  
Roberto Avola ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Antioxidant Properties ◽  
Lactic Dehydrogenase ◽  
Protective Effects ◽  
Astroglial Cells ◽  
Experimental Conditions ◽  
Scavenging Effect ◽  
Cultured Astrocytes ◽  
Diphenyl Tetrazolium Bromide

Background The concentration of peroxynitrite in the brain increases after central nervous system injuries. The authors hypothesized that propofol, because of its particular chemical structure, mitigates the effects of peroxynitrite-mediated oxidative stress and apoptosis by the induction of heme oxygenase (HO)-1 in primary cultured astroglial cells. Methods Primary cultured astroglial cells were incubated for 18 h with a known peroxynitrite donor (3 mm SIN-1) in the presence or absence of propofol (40 microm, 80 microm, 160 microm, and 1 mm). The protective effects of propofol were evaluated by 3(4,5-dimethyl-thiazol-2-yl)2,5-diphenyl-tetrazolium bromide cytotoxicity assay, lactic dehydrogenase release, DNA ladderization by Comet assay, and caspase-3 activation by Western blot analysis. Results Appropriate propofol concentrations (ranging from 40 microm to 1 mm) significantly increased HO-1 expression and attenuated SIN-1-mediated DNA ladderization and caspase-3 activation. The protective effects of propofol were mitigated by the addition of tin mesoporphyrin, a potent inhibitor of HO activity. The addition of a specific synthetic inhibitor of nuclear factor kappaB abolished propofol-mediated HO-1 induction, suggesting a possible role of this nuclear transcriptional factor in our experimental conditions. Conclusions The antioxidant properties of propofol can be partially attributed to its scavenging effect on peroxynitrite as well as to its ability to increase HO-1 expression at higher concentrations, a property that might be relevant to neuroprotection during anesthesia.

scholarly journals Role of Exogenous Hsp72 on Liver Dysfunction during Sepsis

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Tsen-Ni Tsai ◽  
Jia-Jing Ho ◽  
Maw-Shung Liu ◽  
Tzu-Ying Lee ◽  
Mei-Chin Lu ◽  
...  
Keyword(s):  
Liver Dysfunction ◽  
Caspase 3 ◽  
Cecal Ligation ◽  
B Cell Lymphoma ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Caspase 9 ◽  
Protein Expressions ◽  
Glutamate Pyruvate ◽  
Serum Glutamate

This study examined the role of exogenous heat shock protein 72 (Hsp72) in reversing sepsis-induced liver dysfunction. Sepsis was induced by cecal ligation and puncture. Liver function was determined on the basis of the enzymatic activities of serum glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT). Apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3 and caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP) protein expressions were analyzed using Western blotting. Results showed GOT and GPT levels increased during sepsis, and levels were restored following the administration of human recombinant Hsp72 (rhHsp72). Increased liver tissue apoptosis was observed during sepsis, and normal apoptosis resumed on rhHsp72 administration. The Bcl-2/Bax ratio, cleaved caspase-3, caspase-9, and PARP protein expressions in the liver tissues were upregulated during sepsis and normalized after rhHsp72 treatment. We conclude that, during sepsis, exogenous Hsp72 restored liver dysfunction by inhibiting apoptosis via the mitochondria-initiated caspase pathway.

scholarly journals Neuroinflammation trajectories precede cognitive impairment after experimental meningitis—evidence from an in vivo PET study

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Vijayasree V. Giridharan ◽  
Allan Collodel ◽  
Jaqueline S. Generoso ◽  
Giselli Scaini ◽  
Rico Wassather ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Microglial Activation ◽  
Caspase 3 ◽  
Cns Infection ◽  
Control Group ◽  
Caspase 9 ◽  
Activation Markers

Abstract Background Bacterial meningitis is a devastating central nervous system (CNS) infection with acute and long-term neurological consequences, including cognitive impairment. The aim of this study was to understand the association between activated microglia-induced neuroinflammation and post-meningitis cognitive impairment. Method Meningitis was induced in male Wistar rats by injecting Streptococcus pneumoniae into the brain through the cisterna magna, and rats were then treated with ceftriaxone. Twenty-four hours and 10 days after meningitis induction, rats were imaged with positron emission tomography (PET) using [11C]PBR28, a specific translocator protein (TSPO) radiotracer, to determine in vivo microglial activation. Following imaging, the expression of TSPO, cardiolipin, and cytochrome c, inflammatory mediators, oxidative stress markers, and glial activation markers were evaluated in the prefrontal cortex and hippocampus. Ten days after meningitis induction, animals were subjected to behavioral tests, such as the open-field, step-down inhibitory avoidance, and novel object recognition tests. Results Both 24-h (acute) and 10-day (long-term) groups of rats demonstrated increased [11C]PBR28 uptake and microglial activation in the whole brain compared to levels in the control group. Although free from infection, 10-day group rats exhibited increased expression levels of cytokines and markers of oxidative stress, microglial activation (IBA-1), and astrocyte activation (GFAP) similar to those seen in the 24-h group. Acute meningitis induction also elevated TSPO, cytochrome c, and caspase-3 levels with no change in caspase-9 levels. Furthermore, upregulated levels of TSPO, cytochrome c, and caspase-3 and caspase-9 were observed in the rat hippocampus 10 days after meningitis induction with a simultaneous reduction in cardiolipin levels. Animals showed a cognitive decline in all tasks compared with the control group, and this impairment may be at least partially mediated by activating a glia-mediated immune response and upregulating TSPO. Conclusions TSPO-PET could potentially be used as an imaging biomarker for microglial activation and long-term cognitive impairment post-meningitis. Additionally, this study opens a new avenue for the potential use of TSPO ligands after infection-induced neurological sequelae.

Crocin protects against beta-amyloid peptide-induced apoptosis in PC12 cells via PI3 K pathway

2020 ◽  
Vol 13 ◽  
Author(s):  
Reyhaneh Taheri ◽  
Elham Hadipour ◽  
Zahra Tayarani-Najaran
Keyword(s):  
Pc12 Cells ◽  
Caspase 3 ◽  
Beta Amyloid ◽  
Pi3 Kinase ◽  
Amyloid Peptide ◽  
Ros Generation ◽  
Protective Effects ◽  
Beta Amyloid Peptide ◽  
Cyt C ◽  
Induced Apoptosis

Background: Crocin is a known compound with antioxidant and anti-inflammatory property which many help to reduce the progression of neurological disorders. In this study, we aimed to investigate the protective effects of crocin on beta-amyloid peptide Aβ (1-40) and hydrogen peroxide (H2O2) induced neurotoxicity in PC12 cells. Methods: PC12 cells pretreated with crocin and donepezil (5 and 10 µM) for 2 h then treated with Aβ (1-40) (25 µM) for 24 h. In parallel after pretreatment with crocin (5 and 10 µM) and donepezil (5 and 10 µM) for 24 h, cells were treated with H2O2 (800 µM) for 4 h. Finally, the cell viability and intracellular reactive oxygen species (ROS) generation were evaluated using AlamarBlue® and 2', 7'-dichlorodihydrofluorescein diacetate (DCFH-DA), respectively. The western blot test was done to compare the protein level of phospho SAPK/JNK, SAPK/JNK, PI3 Kinase P85, Phospho-PI3 Kinase P85, caspase-3 and cytochrome c )cyt c). Results: Crocin and donepezil could significantly decrease the Aβ toxicity and ROS level. While treatment with Aβ increased Cyt c release from mitochondria to cytosol, cleaved form of caspase-3 (17 kDa) and activated form of SAPK/JNK p44/4 and decreased the activated form of PI3 Kinase P85 protein, crocin could significantly block the apoptosis initiated with Aβ. Conclusions: According to the results crocin could be a promising candidate for further evaluations against the development of Alzheimer's diseases through mitogen-activated protein kinases (MAPK) and the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling (PI3 K/AKT) pathways.

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