Bovine E2 estradiol ELISA Kit (DEIA-BJ2921)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Serum, plasma, cell culture supernatants, body fluid and tissue homogenate
Species Reactivity
Intended Use
Bovine E2 estradiol ELISA Kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of the E2 estradiol. This ELISA kit is for research use only, not for therapeutic or diagnostic applications.
Contents of Kit
2. ENZYME CONJUGATE: 6.0 mL or 10 ml
3. STANDARD A-F: 1 vial each
7. WASH SOLUTION (100 x): 10 mL
All components of this kit are stable at 2-8°C until the kit's expiration date.
Detection Range
250 -5000 pg/mL
1.0 pg/mL


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Evaluation of antioxidant capacity and immunomodulatory effects of yeast hydrolysates for hepatocytes of blunt snout bream (Megalobrama amblycephala)


Authors: Rahimnejad, Samad; Yuan, Xiang-Yang; Liu, Wen-Bin; Jiang, Guang-Zhen; Cao, Xiu-Fei; Dai, Yong-Jun; Wang, Cong-Cong; Desouky, Hesham Eed

An in-vitro study was carried out to examine the effects of yeast hydrolysate (YH) on antioxidant capacity and innate immunity of blunt snout bream (Megalobrama amblycephala) hepatocytes. Fish primary hepatocytes were seeded at a density of 3 x 10(5) cells mL(-1) in 6-well tissue culture plates and treated with two different media including: 1) DMEM/F12 medium (control), and 2) YH medium [DMEM/F12 + 0.1 g L-1 YH]. After incubation for 24 h, the culture medium and primary hepatocytes were collected for subsequent analyses. The results showed no significant (P > 0.05) effect of YH on aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) activities and urea nitrogen (UN) concentration in the conditioned medium. However, significantly (P < 0.05) higher ALT and AST activities were found in YH treated hepatocytes compared to control. Moreover, YH supplementation led to significant enhancement of superoxide dismutase (SOD), catalase (CAT), alternative complement pathway (ACH50) and glutathione peroxidase (GPX) activities and reduction of malondialdehyde (MDA) concentration in the conditioned medium. Furthermore, YH application upregulated the expression of SOD, CAT and NOX2 genes and downregulated mRNA levels of Keap1, Nrf2 and Bach1 in hepatocytes. Also, markedly higher lysozyme activity and albumin concentration were found in the conditioned medium of YH group compared to the control. Additionally, expression of immune-related genes such as antimicrobial peptides 1 (Leap 1) and Leap 2 were significantly upregulated by YH application. Downregulated expression of NADPH oxidase-2 (NOX2), Kelch-like-ECH-associated protein 1 (Keap1), NF-E2-related factor 2 (Nrf2) and BTB and CNC homolog 1 (Bach1) were observed in YH treated hepatocytes. To conclude, YH supplementation improved antioxidant capacity and innate immunity of blunt snout bream hepatocytes.

Role of Interleukin-33 in Staphylococcus epidermidis-Induced Septicemia


Authors: Yang, Min; Wang, Yiwen; Zhang, Yonghong; Li, Yanjun; Li, Qifeng; Tan, Jintong

Interleukin (IL)-33 is a member of the IL-1 family, which plays an important role in inflammatory response. In this study, we evaluated the effect of IL-33 on septicemia and the underlying mechanisms by establishing a Staphylococcus epidermidis (S. epidermidis)-induced septicemic mouse model. The expression of IL-33, IL-1 alpha, IL-1 beta, IL-6, IL-17A, IL-22, and PGE2 were measured by double antibody sandwich enzyme-linked immunosorbent assay, and bacterial colony formation in peripheral blood and kidneys were counted postinfection. The percentages of neutrophils, eosinophils, and inflammatory monocytes were evaluated by flow cytometry, and tissue damage was assessed by hematoxylin and eosin (H&E) staining. The survival of septicemic mice was monitored daily. IL-33 expression was significantly augmented following S. epidermidis infection. High IL-33 expression significantly decreased the survival of model mice, and aggravated the damage of lung, liver, and kidney tissues. However, administration of ST2 (receptor for IL-33) to the S. epidermidis-infected mice blocked the IL-33 signaling pathway, which elevated PGE2, IL-17A, and IL-22, and promoted healing of organ damage. In addition, ST2 suppressed the mobilization of inflammatory monocytes, but promoted the accumulation of neutrophils and eosinophils in S. epidermidis-infected mice. Inhibition of PGE2, IL-17A, and IL-22 facilitated the development of septicemia and organ damage in S. epidermidis-infected mice, as well as reducing their survival. Our findings reveal that IL-33 aggravates organ damage in septicemic mice by inhibiting PGE2, IL-17A, and IL-22 production.

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