Establishment of a hypobaric hypoxia-induced cell injury model in PC12 cells

Objective This study aimed to evaluate the efficacy of Pycnogenol (PYC) and its antioxidant and antiapoptotic effect in an experimental hypoxic-ischemic (HI) rat model. Study Design A total of 24 Wistar albino rats who were on the seventh postnatal day were divided into three groups with developed HI brain injury model under the sevoflurane anesthesia: 40 mg/kg PYC was given to Group A, saline was given to Group B, and the sham group was Group C. Neuronal apoptosis was investigated by terminal deoxynucleotidyl transferase dUTP nick end labeling and immunohistochemically stained manually with primer antibodies of tumor necrosis factor-α and interleukin-1β. Results The neuronal cell injury was statistically lower in the PYC treatment group. Conclusion This is the first study that investigates the role of PYC in the HI brain injury model. PYC reduces apoptosis and neuronal injury in the cerebral tissue of the rats. PYC may be a protective agent against hypoxic-ischemic encephalopathy. Key Points

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Neuroprotective Effect of Cyperi rhizome against Corticosterone-Induced PC12 Cell Injury via Suppression of Ca2+ Overloading

Metabolites ◽

10.3390/metabo9110244 ◽

2019 ◽

Vol 9 (11) ◽

pp. 244 ◽

Cited By ~ 1

Author(s):

Jia ◽

Liu ◽

Yu ◽

Shang ◽

Zhang ◽

...

Keyword(s):

Pc12 Cells ◽

Cell Injury ◽

Cell Damage ◽

Chemical Constituents ◽

Neuroprotective Effect ◽

Vital Role ◽

Emotional Disturbances ◽

Traditional Herbal Medicine ◽

Protection Effect ◽

Independent Protein

Cyperi Rhizoma (CR) is a well-known functional food and traditional herbal medicine in Asian countries for the treatment of menstrual or emotional disturbances in women. Recent studies have shown the pharmacological effects of CR on neuronal diseases, such as Parkinson’s disease (PD) and depression. Thus, the neuroprotective effect of CR might play a vital role in exerting its effect. Here, corticosterone-induced PC12 cells were applied to screen the active fraction of CR and evaluate its neuroprotective effect. The results indicated that the fraction containing medium-polarity chemical constituents (CR-50E) displayed the best protection effect. CR-50E could increase the cell viability and reduce cell apoptosis through inhibiting oxidative stress and decreasing the lactate dehydrogenase LDH release induced by corticosterone. Further, the mechanism of action was explored by cell metabolomics. The result showed CR-50E mediated the sphingolipids metabolism of corticosterone-induced PC12 cells, which suggested inhibition of Ca2+ overloading may involve the protection of CR-50E against cell damage. The expression levels of three key proteins in calcium transport, including phospholipase A2 (PLA2), calcium/calmodulin independent protein kinase II (CaMK II), and caspase-3, confirmed the above result by Western blot. The findings suggest that CR-50E can suppress the disequilibrium of calcium homeostasis-mediated apoptosis by improving the abnormal sphingolipids metabolism as well as remedying the damage of the cell membrane.

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NLRC5 alleviated OGD/R-induced PC12-cell injury by inhibiting activation of the TLR4/MyD88/NF-κB pathway

Journal of International Medical Research ◽

10.1177/0300060520940455 ◽

2020 ◽

Vol 48 (8) ◽

pp. 030006052094045

Author(s):

Zhen Zhang ◽

Yuhan Sun ◽

Xin Chen

Keyword(s):

Cerebral Ischemia ◽

Oxidative Damage ◽

Pc12 Cells ◽

Pc12 Cell ◽

Cell Injury ◽

Inflammatory Responses ◽

Ischemia Reperfusion ◽

Terminal Deoxynucleotidyl Transferase ◽

Enzyme Linked Immunosorbent Assay ◽

Apoptosis Rate

Objective To assess the role of NOD-like receptor C5 (NLRC5; a major NLRC family protein that regulates immunity, inflammation and tissue fibrosis), in cerebral ischemia-reperfusion injury, characterized by inflammation and oxidative damage. Methods Blood NLRC5 levels were assessed in neonates with cerebral ischemia and in healthy controls. A stable PC12 cell line was established that overexpressed or knocked down NLRC5. Inflammatory responses, apoptosis rate and oxidative damage in PC12 cells under oxygen-glucose deprivation/reperfusion (OGD/R) conditions were evaluated using enzyme-linked immunosorbent assay (ELISA), terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) and reactive oxygen species (ROS) assay. Results Blood NLRC5 levels were suppressed in neonates with cerebral ischemia. ELISAs showed that NLRC5 suppressed levels of tumour necrosis factor-α, interleukin (IL)-6, IL-1β, ROS and superoxide dismutase in OGD/R-treated PC12 cells. Furthermore, NLRC5 overexpression was associated with reduced apoptosis rate in PC12 cells treated by OGD/R. Overexpression of NLRC5 also inhibited levels of toll-like receptor (TLR)4, myeloid differentiation primary response protein MyD88 (MyD88) and phosphorylated nuclear factor kappa B-transcription factor p65 (NF-κB p-p65) in PC12 cells, and decreased nuclear levels of NF-κB p-p65. Conclusion NLRC5 alleviated inflammatory responses, oxidative damage and apoptosis in PC12 cells under OGD/R conditions by suppressing activation of the TLR4/MyD88/NF-κB pathway.

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Endothelial Cell Injury Under High Frequency Vibration in the Rat-Tail Model

ASME 2011 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2011-53571 ◽

2011 ◽

Author(s):

Shilpi Goenka ◽

Srikara V. Peelukhana ◽

Jay Kim ◽

Keith F. Stringer ◽

Rupak K. Banerjee

Keyword(s):

Endothelial Cells ◽

Endothelial Cell ◽

Oxidative Damage ◽

Cell Injury ◽

Industrial Workers ◽

Injury Model ◽

Blue Stain ◽

Hematoxylin And Eosin ◽

Rat Tail Model ◽

Rat Tail

Hand-Arm Vibration Syndrome (HAVS) consists of vascular, sensorineural and musculoskeletal disorders and affects around 1.7–5.8% of industrial workers. In this study, a rat-tail vibration injury model is used to assess early vascular damage due to HAVS, manifested in the form of endothelial cell vacuolation and oxidative injury. Tails were vibrated at two frequencies 125Hz and 250Hz for 4hr/day for 1 and 5 days (49m/s2). Hematoxylin and Eosin (H&E) staining was done to assess gross changes in artery sections and toluidine blue stain was done for vacuole counting. Immunohistochemical (IHC) methods were used to detect Nitrotyrosine, a potent biomarker of cell inflammation and oxidative stress. The vacuole count in Endothelial Cells (ECs) was not statistically significant after 1 and 5 days for any frequency. However IHC images showed significant oxidative damage in Endothelial Cells (ECs) with considerable oxidative damage being induced as early as 1 day for both 125Hz and 250Hz frequencies, with more EC damage induced by 250Hz frequency after 5 days. These findings indicate that higher frequency vibrations can cause severe oxidative damage to EC.

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Roles of TRPA1 and TRPV1 in cigarette smoke -induced airway epithelial cell injury model

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2019.01.004 ◽

2019 ◽

Vol 134 ◽

pp. 229-238 ◽

Cited By ~ 17

Author(s):

Muyun Wang ◽

Yanbei Zhang ◽

Mengmeng Xu ◽

Hai Zhang ◽

Yuqing Chen ◽

...

Keyword(s):

Epithelial Cell ◽

Cigarette Smoke ◽

Cell Injury ◽

Airway Epithelial Cell ◽

Airway Epithelial ◽

Injury Model ◽

Epithelial Cell Injury

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Acacetin improves endothelial dysfunction and aortic fibrosis in insulin-resistant SHR rats by estrogen receptors

Molecular Biology Reports ◽

10.1007/s11033-020-05746-3 ◽

2020 ◽

Vol 47 (9) ◽

pp. 6899-6918

Author(s):

Yaxin Wei ◽

Peipei Yuan ◽

Qi Zhang ◽

Yang Fu ◽

Ying Hou ◽

...

Keyword(s):

Estrogen Receptor ◽

Endothelial Cell ◽

Endothelial Dysfunction ◽

Estrogen Receptors ◽

Cell Injury ◽

Shr Rats ◽

Endothelial Cell Injury ◽

Insulin Resistant ◽

Injury Model ◽

Huvec Cells

Abstract The aim of the work was to investigate the effects of acacetin on endothelial dysfunction and aortic fibrosis in insulin-resistant SHR rats and explore its mechanism. Seven-week-old male spontaneously hypertensive rats (SHR) were selected to establish a rat model of hypertension with insulin resistance induced by 10% fructose. The nuclear factor kappa B p65 (NF-κB p65) and Collagen I were observed by Immunohistochemistry. Immunofluorescence was used to observe estrogen receptor-alpha (ERα), estrogen receptor-beta (ERβ), and G protein-coupled receptor 30 (GPR30). Western blotting was used to detect interleukin (IL-1β), Arginase 2 (ARG2), Nostrin, endothelial nitric oxide synthase (eNOS), TGF-β, Smad3, ERK pathway proteins such as p-c-Raf, p-MEK1/2, p-ERK, ERK, p-P90RSK and p-MSK1. We found that acacetin did have an improvement on endothelial dysfunction and fibrosis. Meanwhile, it was also found to have a significant effect on the level of estrogen in this model by accident. Then, the experiment of uterine weight gain in mice confirmed that acacetin had a certain estrogen-like effect in vivo and played its role through the estrogen receptors pathway. In vitro experience HUVEC cells were stimulated with 30 mM/L glucose and 100 mM/L NaCl for 24 h to establish the endothelial cell injury model. HUVEC cells were treated with 1 μM/L estrogen receptors antagonist (ICI 182780) for 30 min before administration. Cell experiments showed that acacetin could reduce the apoptosis of HUVEC cells, the levels of inflammatory cytokines and the expression of TGF-β, Collagen I and Smad3 in endothelial cell injury model. After treatment with ICI 182780, the improvement of acacetin was significantly reversed. The results showed that acacetin relieved endothelial dysfunction and reduced the aortic fibrosis in insulin-resistant SHR rats by reducing the release of inflammatory factors and improving vasodilatory function through estrogen signaling pathway.

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