scholarly journals Shenxiong Drop Pill exerts neuroprotective effect against focal cerebral ischemia partly via regulation of the expressions of ICAM-1 and caspase-3

2021 ◽  
Vol 20 (10) ◽  
pp. 2015-2022
Author(s):  
Shuo-guo Jin ◽  
Ze-ran Chen ◽  
Yang Zhang ◽  
Meng-yuan Huang ◽  
Meng Hou ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Caspase 3 ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Triphenyltetrazolium Chloride ◽  
Scoring Method ◽  
Nissl Staining ◽  
Neuroprotective Effects

Purpose: To investigate the effect of Shenxiong Drop Pill (SXDP) on cerebral infarction (CI) in rats, and the involvement of anti-inflammatory response in the process.Methods: Rats were sacrificed at three different time points, viz, 24, 48 and 72 h after establishment of CI model. Neurological deficit score (NDS) was determined using Bederson’s neurological behavioral scoring method, whereas triphenyltetrazolium chloride (TTC) staining was used to show brain injury. The integrated optical density (IOD) of Nissl bodies and caspase-3-positive nerve cells were measured with Nissl staining and SP kit, respectively. The mRNA expression of intercellular adhesion molecule 1(ICAM-1) was determined using reverse transcription-polymerase chain reaction (RT-PCR).Results: SXDP produced neuroprotective effect at high, medium, and low doses. The infarct volumes in the high-, medium- and low-dose SXDP, and cyclophosphamide groups were significantly reduced at each time point. Different doses of SXDP significantly reduced the mRNA expression of ICAM-1 and the IOD of caspase-3.Conclusion: These results indicate that SXDP exerts neuroprotective effects against ischemic injury by negatively regulating ICAM-1/caspase-3 downstream of inflammatory and apoptosis pathways.

IL-37: Novel neuroprotective effects after brain ischemia and reperfusion

2019 ◽  
Vol 7 (4) ◽  
pp. 310-321
Author(s):  
Huang Xiang ◽  
Stampf Wael
Keyword(s):  
Infarct Size ◽  
Brain Ischemia ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Brain Inflammation ◽  
Mice Model ◽  
Triphenyltetrazolium Chloride ◽  
Nissl Staining ◽  
Neuroprotective Effects

Interleukin-1 (IL-1) is a central mediator of innate immunity and inflammation. IL-37 (IL-37), a newly described member of the IL-1 family, functions as a fundamental inhibitor of innate inflammation and immunity. The purpose of the present study was to determine the effects of interleukin-37 on neuron cells and on brain inflammation induced by brain ischemia/reperfusion (I/R). A transgenic mouse strain was generated to express human IL-37 (hIL-37Tg) and WT mice were subjected to (60 min) brain ischemia and followed by reperfusion (24 h), by using a mice model of transient focal cerebral ischemia induced by advancing a nylon mono-filament to occlude the middle cerebral artery (MCA). Infarct size was determined by triphenyltetrazolium chloride staining. The morphology of neurons in brain sections were examined by Nissl staining and cytokines/chemokines measured by ELIZA. IL-37Tg significantly reduced infarct size by 65.4% (P<0.05) compared with WT after I/R. Reduced inflammation was associated with decreased leukocyte recruitment, and reduced release of IL-1β and TNFα, macrophage inflammatory protein-2 (MIP-2), MCP-1 and keratinocyte chemokine (KC) compared with WT (P<0.05), whereas IL-10 was increased eight fold (P<0.05). IL-37 significantly reduced cell death and increased Bcl-2 expression in neurons. Thus, IL-37 emerges as a key modulator of brain inflammation and has important translational implications for both the prevention and treatment of patients suffering from brain ischemia.

scholarly journals Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Junqiang Yan ◽  
Hongxia Ma ◽  
Xiaoyi Lai ◽  
Jiannan Wu ◽  
Anran Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Protein Expression ◽  
Mitochondrial Membrane Potential ◽  
Western Blotting ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects

Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The oxidative stress is an important component of the pathogenesis of PD. Artemisinin (ART) has antioxidant and neuroprotective effects. The purpose of this study is to explore the neuroprotective effect of ART on 1-methyl-4-phenyliodine iodide (MPP +)-treated SH-SY5Y cells and underlying mechanism. Methods We used MPP+-treated SH-SY5Y cells to study the neuroprotective effect of ART. Cell viability was measured by MTT assay after incubating the cells with MPP+ and/or ART for 24 h. DCFH-DA was used to detect the level of intracellular reactive oxygen species (ROS), and WST-8 was used to detect the level of superoxide dismutase (SOD). The level of intracellular reduced glutathione (GSH) was detected with 5,5΄-dithiobis-(2-nitrobenzoic acid), and the level of malondialdehyde (MDA) was assessed based on the reaction of MDA and thiobarbituric acid. A mitochondrial membrane potential detection kit (JC-1) was used to detect changes in the mitochondrial membrane potential (MMP), and an Annexin V-FITC cell apoptosis kit was used to detect cell apoptosis. The expression levels of caspase-3, cleaved caspase-3 and the autophagy-related proteins LC3, beclin-1, and p62 were detected by Western blotting. In addition, to verify the change in autophagy, we used immunofluorescence to detect the expression of LC3 and p62. Results No significant cytotoxicity was observed at ART concentrations up to 40 μM. ART could significantly increase the viability of SH-SY5Y cells treated with MPP+ and reduce oxidative stress damage and apoptosis. In addition, the Western blotting and immunofluorescence results showed that MPP+ treatment could increase the protein expression of beclin1 and LC3II/LC3I and decrease the protein expression of p62, indicating that MPP+ treatment could induce autophagy. Simultaneous treatment with ART and MPP+ could decrease the protein expression of beclin1 and LC3II/LC3I and increase the protein expression of p62, indicating that ART could decrease the level of autophagy induced by MPP+. Conclusion Our results indicate that ART has a protective effect on MPP+-treated SH-SY5Y cells by the antioxidant, antiapoptotic activities and inhibition of autophagy. Our findings may provide new hope for the prevention and treatment of PD.

Thrombosis and Altered expression of Intercellular Adhesion Molecule-1 (Icam-1) after Avulsion Injury in Rat Vessels

2004 ◽  
Vol 29 (3) ◽  
pp. 228-232 ◽  
Author(s):  
N. ISOGAI ◽  
H. TANAKA ◽  
S. ASAMURA
Keyword(s):  
Mrna Expression ◽  
Adhesion Molecule ◽  
Microscopic Analysis ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Post Injury ◽  
Electron Microscopic ◽  
Altered Expression ◽  
Avulsion Injury

This study was undertaken to characterize the relative degrees of arterial and venous trauma after graded avulsion injuries. Rat femoral arteries and veins were subjected to reproducible avulsion injuries using forces of between 60 and 220 g. Thrombotic occlusion occurred at lower avulsion forces in veins than in arteries. Histologic and scanning electron microscopic analysis indicated increased endothelial disruption and exposed elastic lamina with increasing avulsion force in both vessels, but more prominently in arteries. Intercellular adhesion molecule-1 (ICAM-1) mRNA expression was evident at 3 and 6 hours after avulsion injury in veins, but only with higher avulsion force injuries in arteries. ICAM-1 mRNA expression was not found in either vessel before or after this 3 to 6 hour post-injury interval. These results indicate that the amount of avulsion force to which traumatized extremity vessels are subjected has a direct effect on the degree of intimal injury and subsequent thrombosis.

scholarly journals Tamoxifen Neuroprotection in Cerebral Ischemia Involves Attenuation of Kinase Activation and Superoxide Production and Potentiation of Mitochondrial Superoxide Dismutase

Endocrinology ◽  
2008 ◽  
Vol 149 (1) ◽  
pp. 367-379 ◽  
Author(s):  
Chandramohan Wakade ◽  
Mohammad M. Khan ◽  
Liesl M. De Sevilla ◽  
Quan-Guang Zhang ◽  
Virendra B. Mahesh ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Cerebral Ischemia ◽  
Oxidative Damage ◽  
Caspase 3 ◽  
Focal Cerebral Ischemia ◽  
Artery Occlusion ◽  
Ovariectomized Rats ◽  
Neuroprotective Effects ◽  
Antioxidant Mechanism ◽  
O2 Production

The purpose of this study was to enhance our understanding of the mechanisms of neuronal death after focal cerebral ischemia and the neuroprotective effects of tamoxifen (TMX). The phosphorylation state of 31 protein kinases/signaling proteins and superoxide anion (O2−) production in the contralateral and ipsilateral cortex was measured after permanent middle cerebral artery occlusion (pMCAO) in ovariectomized rats treated with placebo or TMX. The study revealed that pMCAO modulated the phosphorylation of a number of kinases/proteins in the penumbra at 2 h after pMCAO. Of significant interest, phospho-ERK1/2 (pERK1/2) was elevated significantly after pMCAO. TMX attenuated the elevation of pERK1/2, an effect correlated with reduced infarct size. In situ detection of O2− production showed a significant elevation at 1–2 h after pMCAO in the ischemic cortex with enhanced oxidative damage detected at 24 h. ERK activation may be downstream of free radicals, a suggestion supported by the findings that cells positive for O2− had high pERK activation and that a superoxide dismutase (SOD) mimetic, tempol, significantly attenuated pERK activation after MCAO. TMX treatment significantly reduced the MCAO-induced elevation of O2− production, oxidative damage, and proapoptotic caspase-3 activation. Additionally, pMCAO induced a significant reduction in the levels of manganese SOD (MnSOD), which scavenge O2−, an effect largely prevented by TMX treatment, thus providing a potential mechanistic basis for the antioxidant effects of TMX. As a whole, these studies suggest that TMX neuroprotection may be achieved via an antioxidant mechanism that involves enhancement of primarily MnSOD levels, with a corresponding reduction of O2− production, and downstream kinase and caspase-3 activation.

scholarly journals Neuroprotective Effects of Curcumin-Loaded Emulsomes on Laser Axotomy-Induced CNS Injury Model

2020 ◽  
Author(s):  
Elif Nur Yilmaz ◽  
Sadik Bay ◽  
Gurkan Ozturk ◽  
Mehmet Hikmet Ucisik
Keyword(s):  
Hippocampal Neurons ◽  
Caspase 3 ◽  
Ex Vivo ◽  
Neuroprotective Effect ◽  
Axonal Injury ◽  
Survival Rates ◽  
Cns Injury ◽  
Neuroprotective Effects ◽  
Injury Model ◽  
Apoptotic Marker

Abstract Background Curcumin, a polyphenol isolated from the rhizomes of turmeric, holds a great potential as a neuroprotective agent along with its anti-inflammatory and antioxidant characteristics. Its poor bioavailability and low stability in water lie as foremost restraints against the clinical use. This study aims at investigating the neuroprotective effect of curcumin on axonal injury by delivering the lipophilic polyphenol to primary hippocampal neuron by means of a lipid-based drug delivery system, named emulsomes. Methods To study the neuroregeneration on ex vivo, an injury model was established through single-cell laser axotomy on hippocampal neurites. Upon treatment with curcumin-loaded emulsomes (CurcuEmulsomes), curcumin and CurcuEmulsome uptake into neurons were verified by 3-dimensional z-stack images acquired with confocal microscopy. Neuron survival after axonal injury were tracked by PI and Hoechst staining. Alterations in expression levels of physiological markers such as anti-apoptotic marker Bcl-2, apoptotic marker cleaved caspase 3, neuroprotective marker Wnt3a and the neuronal survival marker mTOR were investigated by immunocytochemistry analyses. Results Results indicated significant improvement in the survival rates of injured neurons upon CurcuEmulsome treatment. Bcl-2 expression became significantly higher for injured neurons treated with curcumin or CurcuEmulsome. Caspase 3 expressions decreased in both curcumin- and CurcuEmulsome-treatments, whereas Wnt3a and mTOR expressions did not alter significantly. Conclusions The established laser-axotomy model was exposed as a reliable methodology to study neurodegenerative models ex vivo. CurcuEmulsomes delivered curcumin to primary hippocampal neurons successfully. Treated with CurcuEmulsomes, injured hippocampal neurons benefit from neuroprotective effects of curcumin in terms of higher survival rate and increased anti-apoptotic marker levels.

scholarly journals Sevoflurane Preconditioning against Focal Cerebral Ischemia

2009 ◽  
Vol 110 (6) ◽  
pp. 1271-1278 ◽  
Author(s):  
Jean-Laurent Codaccioni ◽  
Lionel J. Velly ◽  
Chahrazad Moubarik ◽  
Nicolas J. Bruder ◽  
Pascale S. Pisano ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Cerebral Injury ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Sprague Dawley ◽  
Nissl Staining ◽  
Neuroprotective Effects ◽  
Sevoflurane Preconditioning

Background Preconditioning the brain with volatile anesthetics seems to be a viable option for reducing ischemic cerebral injury. However, it is uncertain whether this preconditioning effect extends over a longer period of time. The purpose of this study was to determine if sevoflurane preconditioning offers durable neuroprotection against cerebral ischemia. Methods Rats (Sprague-Dawley) were randomly allocated to two groups: nonpreconditioned control group (n = 44) and preconditioned group (n = 45) exposed to 2.7 vol% sevoflurane (45 min) 60 min before surgery. Animals in both groups were anesthetized with 3.0 vol% sevoflurane and subjected to transient middle cerebral artery occlusion. After 60 min of awake focal ischemia, the filament was removed. Functional neurologic outcome (range 0-18; 0 = no deficit), cerebral infarct size (Nissl staining), and apoptosis (Terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling; cleaved caspase-3 staining) were evaluated at 3, 7, and 14 days after ischemia. Results Sevoflurane preconditioning significantly improved functional outcome and reduced infarct volume (109 +/- 43 vs. 148 +/- 56 mm(3)) 3 days after ischemia compared to the control group. However, after 7- and 14-day recovery periods, no significant differences were observed between groups. The number of apoptotic cells was significantly lower in the preconditioned group than in the control group after 3- and 7-day recovery periods. Fourteen days after ischemia, no differences were observed between groups. Conclusion In this model of transient focal cerebral ischemia, sevoflurane preconditioning induced effective but transient neuroprotective effects. Sevoflurane preconditioning also decreased ischemia-induced apoptosis in a more sustained way because it was observed up to 7 days after injury.

scholarly journals Associations between the ICAM1 gene polymorphisms and atherosclerotic cardiovascular disease risk, including hypercholesterolemia, in rural Thais

2021 ◽  
Author(s):  
Naruemon Wechjakwen ◽  
Amornrat Aroonnual ◽  
Pattaneeya Prangthip ◽  
Ngamphol Soonthornworasiri ◽  
Pornpimol Panprathip Phienluphon ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Mrna Expression ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Intercellular Adhesion Molecule ◽  
Atherosclerotic Cardiovascular Disease ◽  
Nucleotide Polymorphisms ◽  
Intercellular Adhesion Molecule 1 ◽  
Single Nucleotide ◽  
Atherosclerotic Cardiovascular Disease Risk

Abstract We determine the relationships between single nucleotide polymorphisms (SNPs), including rs5498 and rs287432 on Intercellular adhesion molecule 1 gene (ICAM1) and atherosclerotic cardiovascular disease (ASCVD) susceptibility in patients with hypercholesterolemia (HCL). The clinical characteristics of 278 participants were assessed, classified to group having HCL and without HCL. ICAM1 SNPs Genotyping was performed by DNA sequencing and ICAM1 expression was measured using real-time PCR. Positive dominant model rs5498 subjects had twice the risk of HCL (P = 0.005). Participants with the rs5498 AG or GG variants and high ICAM1 mRNA expression (≥ 3.12) had 2.68 times the risk (P = 0.000), and those with a high LDL-C concentration (≥ 3.36 mmol/L) had 1.99 times the risk (P = 0.014) of developing ASCVD compared with those with low ICAM1 mRNA and LDL-C levels. Interestingly, participants carrying the rs5498 AG or GG variants who had tachycardia (resting heart rates (RHRs) > 100 beats/min) had a 5.40-times higher risk than those with a lower RHR (P = 0.010). It may consider the G allele in ICAM1 rs5498 is associated with a higher risk of ASCVD in Thai people with HCL, and is also positively associated with ICAM1 mRNA expression, LDL-C concentration, and RHR.

Rhinovirus infection of primary cultures of human tracheal epithelium: role of ICAM-1 and IL-1β

1997 ◽  
Vol 273 (4) ◽  
pp. L749-L759 ◽  
Author(s):  
Masanori Terajima ◽  
Mutsuo Yamaya ◽  
Kiyohisa Sekizawa ◽  
Shoji Okinaga ◽  
Tomoko Suzuki ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Viral Infection ◽  
Mrna Expression ◽  
Primary Cultures ◽  
Neutralizing Antibody ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Rhinovirus Infection ◽  
Tnf Α ◽  
Viral Titers

Exacerbations of asthma are often associated with respiratory infection caused by rhinoviruses. To study the effects of rhinovirus infection on respiratory epithelium, a primary target for respiratory viruses, human rhinovirus (HRV)-2 and HRV-14 were infected to primary cultures of human tracheal epithelial cells. Viral infection was confirmed by showing that viral titers of supernatants and lysates from infected cells increased with time and by polymerase chain reaction. HRV-2 and HRV-14 infections upregulated the expression of intercellular adhesion molecule-1 (ICAM-1) mRNA, the major rhinovirus receptor, on epithelial cells, and they increased the production of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α in supernatants. Antibodies to ICAM-1 inhibited HRV-14 infection of epithelial cells and decreased the production of cytokines after HRV-14 infection, but they did not alter HRV-2 infection-induced production of cytokines. IL-1β upregulated ICAM-1 mRNA expression and increased susceptibility to HRV-14 infection, whereas other cytokines failed to alter ICAM-1 mRNA expression. Furthermore, a neutralizing antibody to IL-1β significantly decreased viral titers of supernatants and ICAM-1 mRNA expression after HRV-14 infection, but a neutralizing antibody to TNF-α was without effect. Immunohistochemical studies revealed that both HRV-14 infection and IL-1β increased ICAM-1 expression on cultured epithelial cells. These findings imply that HRV-14 infection upregulated ICAM-1 expression on epithelial cells through increased production of IL-1β, thereby increasing susceptibility to infection. These events may be important for amplification of airway inflammation after viral infection in asthma.

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