N1876

Manufactured by Merck Group

Sourced in United States

N1876 is a lab equipment product manufactured by Merck Group. It is designed for general laboratory use. The core function of N1876 is to provide a reliable and precise measurement tool for laboratory applications.

Automatically generated - may contain errors

Lab products found in correlation

M3761, by Merck Group (4 mentions) V2002, by Merck Group (2 mentions) A9518, by Merck Group (2 mentions) A9393, by Merck Group (1 mentions) Methylated bovine serum albumin (mbsa), by Merck Group (1 mentions) Mycobacterium tuberculosis, by BD (1 mentions) F5506, by Merck Group (1 mentions) Neomycin, by Merck Group (1 mentions) Vancomycin, by Merck Group (1 mentions) Metronidazole, by Merck Group (1 mentions)

4 protocols using n1876

Microbiome Modulation in Autoimmune Arthritis

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Naive NOD scid gamma (NSG) mice were either treated with antibiotics: ampicillin (1 g/L, A9393, Sigma-Aldrich), neomycin (1 g/L, N1876, Sigma-Aldrich), metronidazole (1 g/L, M3761, Sigma-Aldrich), and vancomycin (0.5 g/L, V2002, Sigma-Aldrich); or kept on autoclaved water for three weeks. Splenocytes were isolated from arthritic K/BxN mice or NOD controls, pooled, and transferred i.v. (60 million cells/mouse) into control, antibiotics-treated mice or NSG mice reconstituted with gut microbiota from K/BxN or KRN mice as described below.
For bacterial reconstitution, NSG mice were treated with antibiotics for two weeks and changed onto autoclaved water for 24 h before bacterial reconstitution. Feces from arthritic K/BxN or control (naive KRN) mice were collected fresh, homogenized, diluted in PBS and gavaged to NSG mice (0.06 mg feces/mouse) 7 days prior and on the day of cell transfer.

Matei D.E., Menon M., Alber D.G., Smith A.M., Nedjat-Shokouhi B., Fasano A., Magill L., Duhlin A., Bitoun S., Gleizes A., Hacein-Bey-Abina S., Manson J.J., Rosser E.C., Klein N., Blair P.A, & Mauri C. (2021). Intestinal barrier dysfunction plays an integral role in arthritis pathology and can be targeted to ameliorate disease. Med (New York, N.y.), 2(7), 864-883.e9.

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Induction and Measurement of Antigen-Induced Arthritis

Cited 1 time

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AIA was induced as previously described⁴¹ (link)^,⁴² (link). Briefly, mice were immunized subcutaneously at the base of the tail with 200 μg methylated bovine serum albumin (mBSA, Sigma-Aldrich) in 100 μL complete Freund’s adjuvant (CFA) and phosphate-buffered saline (PBS, Sigma-Aldrich). 3 mg/ml CFA was prepared by mixing Mycobacterium tuberculosis (231141, BD) in incomplete Freund’s adjuvant (F5506, Sigma-Aldrich). After 7 days, mice received an intra-articular injection of 200 μg mBSA in 10 μL PBS in the right knee or PBS alone as a control in the left knee. Joint size was measured using calipers. Knee swelling was calculated as percentage increase in size between antigen-injected knee and PBS-injected knee.
Disease scores were calculated as follows:

% S w e l l i n g = \frac{m B S A k n e e - P B S k n e e}{P B S k n e e} \times 100

If treated with antibiotics for microbiota depletion during arthritis, C57BL/6 mice were given, in their drinking water, a combination of neomycin (1 g/L, N1876, Sigma-Aldrich), metronidazole (1 g/L, M3761, Sigma-Aldrich), and vancomycin (0.5 g/L, V2002, Sigma-Aldrich), from 7 days prior to the subcutaneous injection. The mice were kept on antibiotics throughout the experiment.

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Antibiotic Modulation of Animal Gut Microbiome

Cited 1 time

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After 1-wk habituation in the animal facility, animals were randomly assigned for antibiotic-treated or control groups (n = 4 or 5 per cage). As previously reported (50 (link)), a broad-spectrum antibiotic mixture consisting of ampicillin (1 g/L, A9518; Sigma-Aldrich), neomycin (1 g/L, N1876; Sigma-Aldrich), vancomycin (500 mg/L, 94747; Sigma-Aldrich), and metronidazole (1 g/L, M3761; Sigma-Aldrich) was added to the drinking water of the antibiotic-treated group for 4 wk. Due to the large body loss observed in mice treated with metronidazole in drinking water (51 (link)), we opted to gradually increase the concentration of metronidazole over time. In this regime, no metronidazole was added in the first day of treatment; on treatment day 2 metronidazole was introduced in a mass concentration of 250 mg/L, on day 6 the concentration was increased to 500 mg/L, and on day 9 the full concentration (1 g/L) was used. Bottles with antibiotic solution were refilled every week. The control group received regular autoclaved water. Body weight was measured three times per week.

Miller K.A., Vicentini F.A., Hirota S.A., Sharkey K.A, & Wieser M.E. (2019). Antibiotic treatment affects the expression levels of copper transporters and the isotopic composition of copper in the colon of mice. Proceedings of the National Academy of Sciences of the United States of America, 116(13), 5955-5960.

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Antibiotic Treatment and Microbiota Recolonization

Cited 2 times

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Abx treatment was administered according to previously published protocols [54 (link), 56 (link)]. Broad-spectrum Abx mix was diluted in sterilized water and consisted of ampicillin (1 g/L, A9518; Sigma-Aldrich, St. Louis, MO, USA), neomycin (1 g/L, N1876; Sigma-Aldrich), vancomycin (0.5 g/L, 94747; Sigma-Aldrich), and metronidazole (1 g/L, M3761; Sigma-Aldrich). Mice received the Abx solution for at least 14 days. Due to the body weight loss observed at the beginning of the Abx treatment in a pilot experiment (Figure S8), also shown by others [81 (link)], we opted to gradually introduce metronidazole in the Abx solution as previously described [38 (link)]. Briefly, no metronidazole was added on day 0; 0.25 g/L (25% of final concentration) was added at day 2; 0.50 g/L (50% of final concentration) was added at day 6; and 1.0 g/L (full concentration) was added at day 9. Abx solution was refilled every week. Body weight was assessed three times a week to monitor body weight changes. To assess the effects of spontaneous microbiota recolonization, bottles of Abx were swapped for regular autoclaved water at day 14. Mice had access to water for 21 days after the bottle swap to allow for microbiota recolonization.

Vicentini F.A., Keenan C.M., Wallace L.E., Woods C., Cavin J.B., Flockton A.R., Macklin W.B., Belkind-Gerson J., Hirota S.A, & Sharkey K.A. (2021). Intestinal microbiota shapes gut physiology and regulates enteric neurons and glia. Microbiome, 9, 210.

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