Sealed chamber

Manufactured by Embrient Inc

Sourced in United States

The Sealed Chamber is a laboratory equipment designed to provide a controlled and isolated environment for various applications. It is a sealed, airtight enclosure that can maintain specific conditions, such as temperature, humidity, and atmospheric composition. The chamber is constructed with durable materials to ensure containment and isolation within the enclosed space.

Automatically generated - may contain errors

Lab products found in correlation

Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (2 mentions) Dulbecco modified eagle medium (dmem), by Embrient Inc (1 mentions) Ebm 2 basal medium, by Lonza (1 mentions) Endothelial cell growth medium 2, by Lonza (1 mentions)

Spelling variants of this product

Sealed modular incubator chamber (5 citations) Sealed hypoxia chamber (2 citations) Sealed humidified chamber (2 citations)

6 protocols using sealed chamber

OGD-induced Astrocyte Injury Model

Check if the same lab product or an alternative is used in the 5 most similar protocols

The OGD model was established as previously described [16 (link)]. Primary cultured astrocytes were rinsed twice with phosphate-buffered saline (PBS, pH 7.4), and then fresh glucose-free DMEM (11966, Gibco, USA) was added. The cells were placed in a sealed chamber (Billups-Rothenberg, USA), and mixed gas containing 95% N₂ and 5% CO₂ was introduced into the sealed chamber for approximately 10 min to exclude oxygen. Then, the cells were incubated in the sealed hypoxia chamber at 37 °C (the incubation time depended on the experimental requirements). For treatment with Nec-1, 100 μM Nec-1 was added to the astrocytes upon OGD.
RIPK1 or Hsp70.1B knockdown (shRNA RIPK1 or shRNA Hsp70.1B) or control (scr shRNA) lentiviruses were diluted with enhanced infection solution and added to the third passage of primary cultured astrocytes (1 × 10⁸ TU/mL, 10 μL). Then, the cells were transfected for 72 h, and the transfection efficiency was greater than 80%. Western blotting analysis confirmed that RIPK1 (Fig. 1c) and Hsp70.1B (Fig. 4b) were successfully silenced in primary cultured astrocytes.

Du H.P., Guo Y., Zhu Y.M., Gao D.F., Lin B., Liu Y., Xu Y., Said A., Khan T., Liu L.J., Zhu J.J., Ni Y, & Zhang H.L. (2023). RIPK1 inhibition contributes to lysosomal membrane stabilization in ischemic astrocytes via a lysosomal Hsp70.1B-dependent mechanism. Acta Pharmacologica Sinica, 44(8), 1549-1563.

+ Open protocol

+ Expand

In vitro Astrocyte Ischemia-Reperfusion Model

Cited 1 time

Check if the same lab product or an alternative is used in the 5 most similar protocols

To mimic the astrocyte activation after transient cerebral ischemia in vitro, we established the OGD/R model in the primary culture of mice astrocytes according to a previous report [23 (link)]. Briefly, the primary-cultured astrocytes were rinsed twice with phosphate-buffered saline (PBS, pH 7.4), and then refreshed with glucose free DMEM (Gibco). Cells were then placed in a sealed chamber (Billups-Rothenberg, San Diego, CA, USA), loaded with mixed gas containing 95% N₂, and 5% CO₂ at 37 °C for 2–6 h. Following the insult, cultures were transferred back to a DMEM containing 10% FBS and reoxygenated in a humidified incubator (37 °C, 5% CO₂) for an additional 24 h. Cells in the normal control group remained untreated and were incubated in a regular cell culture incubator (37 °C, 5% CO₂). All astrocytes were harvested 24 h after reoxygenation.

Luo D., Ye W., Chen L., Yuan X., Zhang Y., Chen C., Jin X, & Zhou Y. (2023). PPARα Inhibits Astrocyte Inflammation Activation by Restoring Autophagic Flux after Transient Brain Ischemia. Biomedicines, 11(3), 973.

+ Open protocol

+ Expand

Hypoxia and Aglycemia Induction Protocol

Check if the same lab product or an alternative is used in the 5 most similar protocols

Hypoxia was induced by placing cells in a sealed chamber (Billups-Rothenberg Inc.) at 37°C, and introducing a flush with 95% N₂/5% CO₂ gas until the complete removal of O₂. Aglycemia was performed by using RPMI 1640 medium without D-glucose. In experiments related to ischemia without reperfusion, the cells were kept under OGD condition for 6 h. For experiments using OGD and reperfusion (OGD/R) conditions, the cells were kept in OGD for 6 h followed by normal growth condition and normoxic atmosphere for an additional 4 h.

Martins A.H., Hu J., Xu Z., Mu C., Alvarez P., Ford B.D., El Sayed K., Eterovic V.A., Ferchmin P.A, & Hao J. (2015). Neuroprotective Activity of (1S,2E,4R,6R,-7E,11E)-2,7,11-cembratriene-4,6-diol (4R) in vitro and in vivo in Rodent Models of Brain Ischemia. Neuroscience, 291, 250-259.

+ Open protocol

+ Expand

OGD/R-Induced In Vitro Ischemia-Reperfusion Model

Check if the same lab product or an alternative is used in the 5 most similar protocols

the OGD/R model was used to mimic ischemia/reperfusion in vitro. Hypoxia was induced by placing cells in a sealed chamber (BillupsRothenberg, Del Mar, CA) at 37 °C, which has been flushed with 95% N₂ /5% CO₂ gas. The concentration of oxygen in the atmosphere was maintained at 0% oxygen and the PO₂ in the medium was below 25 mmHg. Glycaemia was induced by using RPMI 1640 medium without L-glucose (Hyclone, Logan, UT). After 9 hours OGD, the cells were moved back to normal growth condition for 16 hours. Then the growth medium was changed to serum free medium with the addition of GS24-NFκB or its corresponding controls for another 8 hours. The cell samples were obtained 24 h after re-oxygenation.

Hu J., Al-Waili D., Hassan A., Fan G.C., Xin M, & Hao J. (2016). Inhibition of Cerebral Vascular Inflammation by Brain Endothelium-Targeted Oligodeoxynucleotide Complex. Neuroscience, 329, 30-42.

+ Open protocol

+ Expand

Oxygen-Glucose Deprivation Neuronal Injury Model

Check if the same lab product or an alternative is used in the 5 most similar protocols

Mass cultures (13–14 DIV) were exposed to oxygen-glucose deprivation (OGD), in which original medium containing 25 mM glucose was exchanged for fresh MEM medium with 2.5 mM glucose and exposed to a sealed chamber (Billups-Rothenberg, Del Mar, CA, USA), humidified and saturated with 95% nitrogen and 5% CO₂ at 37°C, for 2.5 h. The gas exchange followed the specifications of the chamber manufacturer (flow of 20 L·min⁻¹ for 4 min to achieve 100% gas exchange). In some experiments, original medium was exchanged for fresh MEM medium containing the specified drugs immediately prior to OGD exposure. Controls were incubated in MEM medium without oxygen deprivation. Following OGD or control treatment, cells were returned to their original medium and incubated under standard culture conditions until the cell death assay (24 h later). We used Hoechst 33342 (5 μM) to identify all nuclei and propidium iodide (PI, 3 μM) for 30 min to stain nuclei of cells with compromised membranes. Mass cultures (10–14 DIV) challenged with H₂O₂ were incubated in 100 μM H₂O₂ for 60 min in the presence of 20 μM MK-801 during and after the insult to ensure no NMDAR contribution to toxicity. After a 24 h latent period cell survival was quantified as for OGD challenge.

Sun M.Y., Taylor A., Zorumski C.F, & Mennerick S. (2017). 24S-hydroxycholesterol and 25-hydroxycholesterol differentially impact hippocampal neuronal survival following oxygen-glucose deprivation. PLoS ONE, 12(3), e0174416.

+ Open protocol

+ Expand

Recombinant ANXA2 Regulates HBMEC Viability

Check if the same lab product or an alternative is used in the 5 most similar protocols

HBMECs were obtained from Cell Systems Corporation (Kirkland, WA, USA). The method of HBMECs culture has been described previously [17] (link). In brief, the cells of passage 6th to 12th were grown with EBM-2 Basal Medium (Lonza, USA) containing Endothelial Cell Growth Medium-2 (Lonza, USA). HBMECs were cultured with RPMI-1640 containing 10% FBS. All cells were kept in a 37 °C humidi ed incubator with 5% CO 2 . HBMEC was treated with indicated concentrations (from 0.1 to 1μg/ml) of recombinant ANXA2. OGD model was used to mimic ischemic stroke in vitro. The cells were cultured with glucose-free RPMI-1640 in a sealed chamber (Billups-Rothenberg, USA) loaded with mixed gas containing 95% N 2 and5% CO 2 for 3 hrs. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenylte-trazolium bromide (MTT) assay was used to evaluate cell viability. Cell viability was expressed as a percentage relative to the normal cells. The data represented 6-12 separate wells assayed per data point, with about 500-1000 cells counted per well.

Lin H., Li W., Shen Z., Bei Y., Wei T., Yu Z., Dai Y, & Dai H. (2023). Annexin A2 promotes angiogenesis after ischemic stroke via annexin A2 receptor - AKT/ERK pathways. Neuroscience letters, 792.

+ Open protocol

+ Expand

About PubCompare

Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.

We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.

However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.

Ready to get started?

Revolutionizing how scientists
search and build protocols!