Ovalbumin (ova)

Manufactured by Merck Group

Sourced in United States, Germany, United Kingdom, China, Sao Tome and Principe, France, Japan, Italy, Switzerland, Denmark, Macao, Canada, Australia, Brazil

The OVA is a laboratory equipment product designed for the detection and analysis of eggs or ova. It provides a reliable and standardized method for sample preparation and observation. The core function of the OVA is to facilitate the identification and quantification of eggs or ova in various samples.

Automatically generated - may contain errors

Lab products found in correlation

Aluminum hydroxide, by Merck Group (86 mentions) Bovine serum albumin (bsa), by Merck Group (74 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (37 mentions) Imject alum, by Thermo Fisher Scientific (36 mentions) Ovalbumin (ova), by Thermo Fisher Scientific (28 mentions) Lipopolysaccharides (lps), by Merck Group (25 mentions) Dexamethasone (dex), by Merck Group (23 mentions) Aluminum hydroxide, by Thermo Fisher Scientific (22 mentions) Complete freund s adjuvant, by Merck Group (20 mentions) Incomplete freund s adjuvant, by Merck Group (17 mentions) Ova grade 5, by Merck Group (17 mentions) Dimethyl sulfoxide (dmso), by Merck Group (15 mentions) Phosphate buffered saline (pbs), by Merck Group (14 mentions) Carbonic anhydrase, by Merck Group (12 mentions) Ovalbumin (ova), by BD (12 mentions) Methacholine, by Merck Group (12 mentions) Pierce bca protein assay kit, by Thermo Fisher Scientific (12 mentions) Alum adjuvant, by Thermo Fisher Scientific (11 mentions) Imject alum adjuvant, by Thermo Fisher Scientific (11 mentions) Tween 20, by Merck Group (10 mentions)

1 263 protocols using ovalbumin (ova)

Establishment of Xenograft Tumor Model for OVA and ABP-AW1 Study

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To establish xenograft tumors, E.G7-OVA cells in the log phase of growth were washed once with serum-free RPMI-1640 medium and resuspended in 10 ml fresh serum-free RPMI-1640 medium at 5×10⁶ cells/ml. A total of 5×10⁵ cells were then injected subcutaneously into the right lateral thighs of the mice.
After inoculation with the E.G7-OVA cells, all mice were randomly divided into 5 groups of 10 mice each. On days 3, 10 and 17 post-inoculation, the mice received a subcutaneous injection of 100 µl PBS (for PBS group), 100 µl PBS containing 100 µg OVA (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany; for OVA-alone group), or 100 µg OVA together with 50, 100 or 200 µg ABP-AW1 (for low-, intermediate-, or high-dose OVA and ABP-AW1 groups, respectively).
From day 7 after tumor cell inoculation, tumor growth in all groups was monitored every two days by measuring the length (L) and width (W) of the growing nodule, and the volume (V) was calculated as V = (L × W²)/2.
On day 28 after tumor inoculation, all mice were euthanized and no mice presented signs of distress, cachexia or ulceration on the tumors. The tumor was isolated and weighed, and other tissues including the spleen and the peripheral blood were collected for further experiments.

Jiang L., Yu Z., Lin Y., Cui L., Yao S., Lv L, & Liu J. (2018). Low-molecular-weight polysaccharides from Agaricus blazei Murrill modulate the Th1 response in cancer immunity. Oncology Letters, 15(3), 3429-3436.

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Huai Qi Huang Alleviates Ovalbumin-Induced Asthma in Mice

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Mice were randomly divided into four groups (n=10 in each group): the control group, the OVA group, OVA mice that were treated with Huai Qi Huang (OVA + Huai Qi Huang group), and OVA mice that were treated with dexamethasone (Dex) (OVA + Dex). Dex is widely used to treat asthma and served as a positive control in the present study. Mice in the last three groups were intraperitoneally (i.p.) injected with 100 μg OVA (Sigma, St. Louis, MO, U.S.A.) emulsified in 1 mg aluminum hydroxide (Pierce Chemical Co., Rockford, IL, U.S.A.) with a total volume of 0.2 ml on days 0–14. One day later, mice were challenged for 30 min via the airway with OVA (5% OVA) by ultrasonic nebulizer each day on days 15–22 consecutively. In the OVA + Huai Qi Huang group, OVA-treated mice were administered with Huai Qi Huang (0.4 g/100 g body weight; Qidong Gaitianli Pharmaceutical Co., Ltd, Zhunzi, B20020074) daily by intragastric gavage. In the OVA + Dex group, OVA-treated mice were administered Dex phosphate (Sigma, 10% solution in PBS) by intragastric gavage for 1 h before OVA aerosol on days 15–22. Mice in the control group received the same schedule for sensitization and were administered with an equivalent amount of 0.9% sterile saline instead of OVA.

Liang P., Peng S., Zhang M., Ma Y., Zhen X, & Li H. (2017). Huai Qi Huang corrects the balance of Th1/Th2 and Treg/Th17 in an ovalbumin-induced asthma mouse model. Bioscience Reports, 37(6), BSR20171071.

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OVA-induced Acute Allergic Airway Inflammation

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OVA-induced acute allergic airway inflammation model was established as reported in our previous study [41 (link),42 (link)]. On days 0 and 7, mice were sensitized with 0.5 mL suspension consisting of 10 μg OVA (Sigma-Aldrich, St. Louis, MO, USA) and 1 mg KAl (SO4)₂ (Sangon Biotech, Shanghai, China) in saline intraperitoneally. Between day 14 and 20, mice were challenged by airway inhalation for 30 min with 1% OVA every day, the time of allergen challenge was among 5:00–7:00 p.m. due to mice showed a strong time-of-day response in features of airway inflammation [9 ,30 ]. Vehicle mice received inhalation of equivalent saline. Mice were randomly grouped, in OVA plus melatonin group and OVA plus Luzindole group, melatonin (10 mg/kg, Sigma) or Luzindole (30 mg/kg, Sigma) was intraperitoneally injected 1 h before OVA challenge for consecutive 7 days, respectively (supplementary file 1: Fig. S3).

Guo S.N., Jiang X.Q., Chen N., Song S.M., Fang Y., Xie Q.M., Fei G.H, & Wu H.M. (2024). Melatonin regulates circadian clock proteins expression in allergic airway inflammation. Heliyon, 10(6), e27471.

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Allergic Airway Inflammation Model with CpG-ODN and SP600125

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Acute allergic airway inflammation was induced according to our previous study and modified.30 (link) On Day 0 and 7, mice were sensitized with 0.5 mL suspension consisting of 10 μg OVA (Sigma) and 1 mg KAl(SO4)₂ (Sangon Biotech, Shanghai, China) in saline intraperitoneally. Then from Day 14 to 20, mice were challenged with 1% OVA by airway inhalation 30 min every day. The mice were randomly grouped into two parts. Part 1 comprised four groups (control, CpG-ODN, OVA, OVA + CpG-ODN), n = 6 for each; Part 2 comprised four groups (OVA, OVA + SP600125, OVA + CpG-ODN, OVA + CpG-ODN + SP600125), n = 6 for each. For CpG-ODN, OVA + CpG-ODN and OVA + CpG-ODN + SP600125 groups, 30 μg of CpG-ODN were given intraperitoneally to mice one hour before OVA challenge. For OVA + SP600125, OVA + CpG-ODN + SP600125 groups, SP600125 (30 mg/kg, Sigma) were given intraperitoneally to mice two hours before OVA challenge.

Zhang H.Y., Xie Q.M., Zhao C.C., Sha J.F., Ruan Y, & Wu H.M. (2021). CpG Oligodeoxynucleotides Attenuate OVA-Induced Allergic Airway Inflammation via Suppressing JNK-Mediated Endoplasmic Reticulum Stress. Journal of Asthma and Allergy, 14, 1399-1410.

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Murine Asthma Model for Immunomodulation

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Asthma was induced in mice as described previously.21 (link) In brief, mice were randomly divided into four groups, namely, PBS, OVA, OVA/PBS, and OVA/SJMHE1 group. On days 0, 7, and 14, each mouse in PBS group was immunized by intraperitoneal injection of 200 µL of PBS, while the mice in the other groups were immunized by 50 µg OVA (Sigma-Aldrich, Steinheim, Germany) and 2 mg of 10% aluminum hydroxide gel in PBS. On days 14 and 21, mice in OVA/PBS and OVA/SJMHE1 groups were separately treated with PBS and SJMHE1 (10 µg) emulsified with incomplete Freund’s adjuvant (Sigma, Poole, UK) as described previously.21 (link) On days 21–28, the mice were challenged in the form of atomization with OVA (2%) or PBS as previously described.21 (link) All the mice were sacrificed on the day 29 to evaluate airway inflammation and immune response.

Li L., Shan W., Zhu H., Xue F., Ma Y., Dong L., Feng D., Mao J., Yuan G, & Wang X. (2021). SJMHE1 Peptide from Schistosoma japonicum Inhibits Asthma in Mice by Regulating Th17/Treg Cell Balance via miR-155. Journal of Inflammation Research, 14, 5305-5318.

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Ovalbumin-Induced Asthma Model in Mice

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C57 mice were obtained from Shanghai Slac Laboratory Animal Company Limited (Co. Ltd) and the asthma model was established in mice using OVAlbumin (OVA). In brief, mice (n=8 for each group) were sensitized with 10 mg OVA (#S7591, Sigma-Aldrich, USA) and 1 mg aluminum hydroxide was dissolved in 500 μL saline intraperitoneally on day 0 and day 7. From day 14 to 16, mice were exposed to OVA nebulization in saline solution (1% w/v) for 30 min. Each animal was challenged using an ultrasonic nebulizer with a flow rate of 1 ml/min. Animals were divided into 4 groups (10 mice/group): Vehicle, OVA, OVA+ 2.5 mg/kg HNG (#H6161, Sigma-Aldrich, USA), and OVA+ 5 mg/kg HNG. Animals in the OVA group were treated according to the procedure described above. In the vehicle group, healthy mice were sensitized with 1 mg aluminum hydroxide on day 0 and day 7, followed by being treated with saline aerosol for 30 min from day 14 to 16. Mice in the OVA+ 2.5 mg/kg HNG and OVA+ 5 mg/kg HNG group were treated (i.p) daily with 2.5 mg/kg and 5 mg/kg HNG from day 0 to day 16 [21 (link)], respectively.

Su B., Li R., Song F., Liu M, & Sun X. (2023). S14G-Humanin ameliorates ovalbumin-induced airway inflammation in asthma mediated by inhibition of toll-like receptor 4 (TLR4) expression and the nuclear factor κ-B (NF-κB)/early growth response protein-1 (Egr-1) pathway. Aging (Albany NY), 15(14), 6822-6833.

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Fisetin Alleviates OVA-Induced Asthma in Mice

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Forty male C57BL/6 mice weighing 20–25 g were obtained from Nanjing Medical university (Nanjing, China). The mice were maintained in a room temperature at 25±2°C and relative 50±5% humidity-controlled environment with a standard cycle of 12 h light/dark. The model animals were administered standard diet and water ad libitum provided in the cages. The experimental procedures of this study were approved by the ethics Committee on Animal Research at Qinhuangdao First Hospital (Hebei, China). The mice in the experiments were divided into 4 groups randomly as follows: i) the control group (Con); ii) the OVA (Sigma-Aldrich, St. Louis, MO, USA)-induced group (Mod); iii) 40 mg/kg fisetin-treated OVA-induced group (FL); and iv) 50 mg/kg fisetin-treated OVA-induced group (FH). OVA was purchased from Sigma-Aldrich.

Huang W., Li M.L., Xia M.Y, & Shao J.Y. (2018). Fisetin-treatment alleviates airway inflammation through inhbition of MyD88/NF-κB signaling pathway. International Journal of Molecular Medicine, 42(1), 208-218.

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Allergic Airway Inflammation Modulation

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BALB/c mice were divided into four treatment groups of 10 mice each as follows: (1) control group mice, sensitized and challenged with saline (group A), (2) OVA group mice, sensitized and challenged with OVA (group B), (3) isotype group mice, treated with isotype Abs for anti-IL-9 (group C), and (4) anti-IL-9 group mice, treated with an anti-IL-9 Ab (group D).
The OVA group mice were sensitized on days 0, 2, 4, 6, 8, 10, 12, and 14 by intraperitoneal (i.p.) injection with 1 mg/mL OVA (Sigma-Aldrich, St. Louis, MO, USA) and 20 mg/mL aluminum hydroxide (Sigma-Aldrich) in saline at a dose of 100 μL/mouse.
After 2 weeks, the animals were challenged by daily nasal instillation of 100 μg OVA in 20 μL saline per mouse, by means of a micropipette, from day 15 to day 25.
Mice from the isotype group and the anti-IL-9 group were given intranasal instillations of hamster IgG (isotype Ab for anti-IL-9, eBioscience, San Diego, CA, USA) and anti-IL-9 Abs (eBioscience), respectively, 30 min prior to the OVA challenge, at a dose of 10 μg in 20 μL saline per mouse. Control group mice were sensitized and challenged with saline instead of OVA at all stages.

Gu Z.W., Wang Y.X, & Cao Z.W. (2017). Neutralization of interleukin-9 ameliorates symptoms of allergic rhinitis by reducing Th2, Th9, and Th17 responses and increasing the Treg response in a murine model. Oncotarget, 8(9), 14314-14324.

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Hyperimmunized Mouse Protocol for Ovalbumin

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All mouse experiments were performed under the guidelines and protocols approved by the Basel-Stadt cantonal veterinary office (Protocol #2582). Female BALB/c mice (Charles River) were housed under specific pathogen–free conditions. Untreated mice (n = 3) were received at age 3 weeks and housed for 9 weeks before being sacrificed. Hyperimmunized mice were received at age 6 weeks and were injected a week later with 150 μl of a PBS-based solution consisting of the following: (day 0) primary subcutaneous injection containing 200 μg of ovalbumin (Sigma, A5503) and 20 μg of adjuvant monophosphoryl lipid A (MPLA; Sigma, L6895), two booster injections at days 21 and 42 with 50 μg of ovalbumin and 20 μg of MPLA, and a final intraperitoneal booster injection at day 61 with 50 μg of ovalbumin (no adjuvant). Mice were sacrificed 10 days after the final injection. At the time of sacrifice, spleens were removed and placed directly in 1.5 ml of RNAlater (Sigma, R0901), stored overnight at 4°C, and moved to −20°C and stored until further processing.

Khan T.A., Friedensohn S., de Vries A.R., Straszewski J., Ruscheweyh H.J, & Reddy S.T. (2016). Accurate and predictive antibody repertoire profiling by molecular amplification fingerprinting. Science Advances, 2(3), e1501371.

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Ovalbumin-Induced Airway Inflammation Model

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Balb/C mice were sensitized to ovalbumin on day 0 and 7 with an i.p. injection of 8 μg ovalbumin (Sigma-Aldrich, St. Louis, MO) in 2 mg Alum Imject (Thermo-Fisher-Scientific, Waltham, MA). On days 14 and 16, animals received intra-nasal challenge of 0.3 μg ovalbumin or 0.3 μg ovalbumin/100 ng LPS (Sigma-Aldrich, St. Louis, MO). On day 17 the lungs were lavaged 3 times with 0.5 ml PBS/EDTA (Invitrogen, Carlsbad, CA) and the lavage fluid pooled and a cell pellet collected by centrifugation for flow cytometric analysis. Mice were treated orally with indicated doses of A-1396076 BID or with 3 mg/kg dexamethasone beginning on day 13 prior to intranasal challenge. Flow cytometric analysis of bronchoalveolar pellets was performed using anti-CD11c APC, anti-CD80 PCP-Cy5.5, anti-CD86 PE, and anti-MHC Class II FITC antibodies (BD Biosciences, San Jose, CA).

Goess C., Terrillon S., Mayo M., Bousquet P., Wallace C., Hart M., Mathieu S., Twomey R., Donnelly-Roberts D., Namovic M., Jung P., Hu M., Richardson P., Esbenshade T, & Cuff C.A. (2020). NRF2 activator A-1396076 ameliorates inflammation in autoimmune disease models by inhibiting antigen dependent T cell activation. Journal of Translational Autoimmunity, 4, 100079.

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