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cholesterol tc colorimetric assay kits  (Elabscience Biotechnology)


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    Structured Review

    Elabscience Biotechnology cholesterol tc colorimetric assay kits
    Cholesterol Tc Colorimetric Assay Kits, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 129 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/total+cholesterol+kit/Total+Cholesterol+(TC)+Colorimetric+Assay+Kit+(Single+Reagent/pmc13102662-76-13-19
    Average 95 stars, based on 129 article reviews
    cholesterol tc colorimetric assay kits - by Bioz Stars, 2026-10
    95/100 stars

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    Related Articles

    Colorimetric Assay:

    Article Title: Redistribution of branched-chain amino acid intake between active and inactive phases modulates hepatic metabolism in rats
    Article Snippet: Biomarker assays were performed using commercially available kits from Elabscience (Wuhan, China) following the manufacturers’ protocols. .. Specifically, serum lipids were quantified by measuring total cholesterol (TC) using the Total Cholesterol (TC) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K109-M), high-density lipoprotein cholesterol (HDL-C) using the HDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K221-M), low-density lipoprotein cholesterol (LDL-C) using the LDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K205-M), malondialdehyde (MDA) using the Malondialdehyde (MDA) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K025-M), and triglycerides (TGs) using the Triglyceride (TG) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K261-M). .. Additionally, total superoxide dismutase (T-SOD) activity was measured using the T-SOD Activity Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K019-M), and total/oxidized glutathione was assessed using the Total Glutathione (T-GSH)/Oxidized Glutathione (GSSG) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K097-M).

    Article Title: A feed-forward loop between niche adenosine and Gzmk⁺ CD8 T cells propagates systemic inflammaging
    Article Snippet: Plasma activities of alanine aminotransferase (ALT/GPT) and aspartate aminotransferase (AST/GOT) in mice were measured using ALT Activity Assay Kit (E-BC-K235-M, Elabscience) and AST Activity Assay Kit (E-BC-K236-M, Elabscience), respectively. .. Total cholesterol (TC) levels in mouse plasma were determined using a colorimetric assay kit (E-BC-K109-M, Elabscience). .. Plasma concentrations of IL-6 and TNF-α in mice were quantified using mouse micro-sample IL-6 ELISA kit (E-MSEL-M0001, Elabscience) and mouse micro-sample TNF-α ELISA kit (E-MSEL-M0002, Elabscience), respectively.

    Multiple Displacement Amplification:

    Article Title: Redistribution of branched-chain amino acid intake between active and inactive phases modulates hepatic metabolism in rats
    Article Snippet: Biomarker assays were performed using commercially available kits from Elabscience (Wuhan, China) following the manufacturers’ protocols. .. Specifically, serum lipids were quantified by measuring total cholesterol (TC) using the Total Cholesterol (TC) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K109-M), high-density lipoprotein cholesterol (HDL-C) using the HDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K221-M), low-density lipoprotein cholesterol (LDL-C) using the LDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K205-M), malondialdehyde (MDA) using the Malondialdehyde (MDA) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K025-M), and triglycerides (TGs) using the Triglyceride (TG) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K261-M). .. Additionally, total superoxide dismutase (T-SOD) activity was measured using the T-SOD Activity Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K019-M), and total/oxidized glutathione was assessed using the Total Glutathione (T-GSH)/Oxidized Glutathione (GSSG) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K097-M).

    other:

    Article Title: Effects of Guanxinning tablet on the gut microbiota and bile acid metabolism in mice with hyperlipidemia
    Article Snippet: The levels of total cholesterol (TC) (E-BC-K109-M), triglycerides (TG) (E-BC-K251-M), high-density lipoprotein cholesterol (HDL-C) (E-BC-K221-M), low-density lipoprotein cholesterol (LDL-C) (E-BC-K205-M) and D-Lactic Acid (D-LA) (E-BC-K002-M) in the serum were measured using colorimetric assays using commercial kits (Elabscience, Wuhan, China).

    Clinical Proteomics:

    Article Title: A feed-forward loop between niche adenosine and Gzmk⁺ CD8 T cells propagates systemic inflammaging
    Article Snippet: Plasma activities of alanine aminotransferase (ALT/GPT) and aspartate aminotransferase (AST/GOT) in mice were measured using ALT Activity Assay Kit (E-BC-K235-M, Elabscience) and AST Activity Assay Kit (E-BC-K236-M, Elabscience), respectively. .. Total cholesterol (TC) levels in mouse plasma were determined using a colorimetric assay kit (E-BC-K109-M, Elabscience). .. Plasma concentrations of IL-6 and TNF-α in mice were quantified using mouse micro-sample IL-6 ELISA kit (E-MSEL-M0001, Elabscience) and mouse micro-sample TNF-α ELISA kit (E-MSEL-M0002, Elabscience), respectively.

    Article Title: Hepatic IFRD1 suppresses metabolic dysfunction-associated fatty liver disease via GLUD1/α-KG axis
    Article Snippet: Journal Pre-proofs Article Hepatic IFRD1 suppresses metabolic dysfunction-associated fatty liver dis‐ ease via GLUD1/α-KG axis Mengya Geng, Fanzheng Meng, Hairui Li, Lijie Sun, Xuedan Sun, Yu Ding, Rongdongqing Shi, Zhihua Wang, Yabin Huang, Jizhou Wang, Yao Liu, Jiabei Wang, Peter J.. Little, Suowen Xu, Lianxin Liu, Jianping Weng, Sihui Luo PII: S2095-9273(26)00365-8 DOI: https://doi.org/10.1016/j.scib.2026.04.016 Reference: SCIB 3996 To appear in: Science Bulletin Received Date: 28 October 2025 Revised Date: 24 February 2026 Accepted Date: 3 April 2026 Please cite this article as: M. Geng, F. Meng, H. Li, L. Sun, X.. Sun, Y. Ding, R. Shi, Z. Wang, Y. Huang, J. Wang, Y. Liu, J. Wang, P.J.

    AST Assay:

    Article Title: Hepatic IFRD1 suppresses metabolic dysfunction-associated fatty liver disease via GLUD1/α-KG axis
    Article Snippet: Journal Pre-proofs Article Hepatic IFRD1 suppresses metabolic dysfunction-associated fatty liver dis‐ ease via GLUD1/α-KG axis Mengya Geng, Fanzheng Meng, Hairui Li, Lijie Sun, Xuedan Sun, Yu Ding, Rongdongqing Shi, Zhihua Wang, Yabin Huang, Jizhou Wang, Yao Liu, Jiabei Wang, Peter J.. Little, Suowen Xu, Lianxin Liu, Jianping Weng, Sihui Luo PII: S2095-9273(26)00365-8 DOI: https://doi.org/10.1016/j.scib.2026.04.016 Reference: SCIB 3996 To appear in: Science Bulletin Received Date: 28 October 2025 Revised Date: 24 February 2026 Accepted Date: 3 April 2026 Please cite this article as: M. Geng, F. Meng, H. Li, L. Sun, X.. Sun, Y. Ding, R. Shi, Z. Wang, Y. Huang, J. Wang, Y. Liu, J. Wang, P.J.

    Article Title: Odevixibat ameliorates high-fat diet-induced MASLD in mice by targeting the gut microbiota-metabolite axis and enhancing gut-liver crosstalk.
    Article Snippet: (MASH), advanced fibrosis, or even cirrhosis [2].. MASLD prevalence is tightly linked to obesity, insulin resistance, and metabolic syndrome, reflecting the intricate interplay between genetic, environmental, and lifestyle factors [2].. The alarming rise in MASLD incidence underscores the urgent need for a comprehensive understanding of its pathogenesis, risk factors, and underlying mechanisms.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Odevixibat ameliorates high-fat diet-induced MASLD in mice by targeting the gut microbiota-metabolite axis and enhancing gut-liver crosstalk.
    Article Snippet: (MASH), advanced fibrosis, or even cirrhosis [2].. MASLD prevalence is tightly linked to obesity, insulin resistance, and metabolic syndrome, reflecting the intricate interplay between genetic, environmental, and lifestyle factors [2].. The alarming rise in MASLD incidence underscores the urgent need for a comprehensive understanding of its pathogenesis, risk factors, and underlying mechanisms.



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    NPC1 disrupts cellular <t>cholesterol</t> distribution. (A) Wild-type and NPC1 knockout HeLa cells were treated with U18666A (10 µM) and HTNV (MOI = 10), cellular cholesterol levels were measured at 48 h post-infection. Non-treatment, U18666A treatment only or HTNV infection only were all parallel control. (B) Wild-type and NPC1 knockout HeLa cells were treated with cholesterol (10 µM) and HTNV (MOI = 1) or not, and viral genome copies within medium and cells of each group were quantified using qPCR. (C) The cellular cholesterol distribution of each group was visualized by Filipin staining following the same treatment as (A) . (D) The represented captures of Filipin staining for each group. WT: wild type HeLa cells, KO: NPC1 knockout HeLa cells. Mock+DMSO: cells were treated with the same amount of DMSO and without HTNV infection; Mock+U18666A: cells were treated with10 μM U18666A and without HTNV infection; HTNV+DMSO: cells treated with the same amount of DMSO and with HTNV infection for 48 hours (MOI=1); HTNV+U18666A: cells were treated with10 μM U18666A andwith HTNV infection for 48 hours (MOI=1).
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    NPC1 disrupts cellular <t>cholesterol</t> distribution. (A) Wild-type and NPC1 knockout HeLa cells were treated with U18666A (10 µM) and HTNV (MOI = 10), cellular cholesterol levels were measured at 48 h post-infection. Non-treatment, U18666A treatment only or HTNV infection only were all parallel control. (B) Wild-type and NPC1 knockout HeLa cells were treated with cholesterol (10 µM) and HTNV (MOI = 1) or not, and viral genome copies within medium and cells of each group were quantified using qPCR. (C) The cellular cholesterol distribution of each group was visualized by Filipin staining following the same treatment as (A) . (D) The represented captures of Filipin staining for each group. WT: wild type HeLa cells, KO: NPC1 knockout HeLa cells. Mock+DMSO: cells were treated with the same amount of DMSO and without HTNV infection; Mock+U18666A: cells were treated with10 μM U18666A and without HTNV infection; HTNV+DMSO: cells treated with the same amount of DMSO and with HTNV infection for 48 hours (MOI=1); HTNV+U18666A: cells were treated with10 μM U18666A andwith HTNV infection for 48 hours (MOI=1).
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    NPC1 disrupts cellular <t>cholesterol</t> distribution. (A) Wild-type and NPC1 knockout HeLa cells were treated with U18666A (10 µM) and HTNV (MOI = 10), cellular cholesterol levels were measured at 48 h post-infection. Non-treatment, U18666A treatment only or HTNV infection only were all parallel control. (B) Wild-type and NPC1 knockout HeLa cells were treated with cholesterol (10 µM) and HTNV (MOI = 1) or not, and viral genome copies within medium and cells of each group were quantified using qPCR. (C) The cellular cholesterol distribution of each group was visualized by Filipin staining following the same treatment as (A) . (D) The represented captures of Filipin staining for each group. WT: wild type HeLa cells, KO: NPC1 knockout HeLa cells. Mock+DMSO: cells were treated with the same amount of DMSO and without HTNV infection; Mock+U18666A: cells were treated with10 μM U18666A and without HTNV infection; HTNV+DMSO: cells treated with the same amount of DMSO and with HTNV infection for 48 hours (MOI=1); HTNV+U18666A: cells were treated with10 μM U18666A andwith HTNV infection for 48 hours (MOI=1).
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    Image Search Results


    NPC1 disrupts cellular cholesterol distribution. (A) Wild-type and NPC1 knockout HeLa cells were treated with U18666A (10 µM) and HTNV (MOI = 10), cellular cholesterol levels were measured at 48 h post-infection. Non-treatment, U18666A treatment only or HTNV infection only were all parallel control. (B) Wild-type and NPC1 knockout HeLa cells were treated with cholesterol (10 µM) and HTNV (MOI = 1) or not, and viral genome copies within medium and cells of each group were quantified using qPCR. (C) The cellular cholesterol distribution of each group was visualized by Filipin staining following the same treatment as (A) . (D) The represented captures of Filipin staining for each group. WT: wild type HeLa cells, KO: NPC1 knockout HeLa cells. Mock+DMSO: cells were treated with the same amount of DMSO and without HTNV infection; Mock+U18666A: cells were treated with10 μM U18666A and without HTNV infection; HTNV+DMSO: cells treated with the same amount of DMSO and with HTNV infection for 48 hours (MOI=1); HTNV+U18666A: cells were treated with10 μM U18666A andwith HTNV infection for 48 hours (MOI=1).

    Journal: Frontiers in Immunology

    Article Title: NPC1 promotes HTNV replication by controlling innate immune response

    doi: 10.3389/fimmu.2026.1811629

    Figure Lengend Snippet: NPC1 disrupts cellular cholesterol distribution. (A) Wild-type and NPC1 knockout HeLa cells were treated with U18666A (10 µM) and HTNV (MOI = 10), cellular cholesterol levels were measured at 48 h post-infection. Non-treatment, U18666A treatment only or HTNV infection only were all parallel control. (B) Wild-type and NPC1 knockout HeLa cells were treated with cholesterol (10 µM) and HTNV (MOI = 1) or not, and viral genome copies within medium and cells of each group were quantified using qPCR. (C) The cellular cholesterol distribution of each group was visualized by Filipin staining following the same treatment as (A) . (D) The represented captures of Filipin staining for each group. WT: wild type HeLa cells, KO: NPC1 knockout HeLa cells. Mock+DMSO: cells were treated with the same amount of DMSO and without HTNV infection; Mock+U18666A: cells were treated with10 μM U18666A and without HTNV infection; HTNV+DMSO: cells treated with the same amount of DMSO and with HTNV infection for 48 hours (MOI=1); HTNV+U18666A: cells were treated with10 μM U18666A andwith HTNV infection for 48 hours (MOI=1).

    Article Snippet: Wild-type and NPC1 knockout HeLa cells were grown on a six-well plate for 12 h, 10 μM U18666A and HTNV (MOI = 1) were added to the cells, and the cellular cholesterol level was measured using Tissue Total Cholesterol (TC) Content Assay Kit (APPLYGEN) at 48 h post-infection.

    Techniques: Knock-Out, Infection, Control, Staining

    Diagram of NPC1 functioning in HTNV life cycle. HTNV infection triggers cellular cholesterol redistribution, which requires NPC1. Cholesterol extensively accumulated in late-endosome, thereby amplifying the innate immune response, when HTNV infected NPC1 defective cells. Consequently, NPC1 avoids abnormal endosomal cholesterol accumulation to mitigate innate immune response and promote HTNV replication.

    Journal: Frontiers in Immunology

    Article Title: NPC1 promotes HTNV replication by controlling innate immune response

    doi: 10.3389/fimmu.2026.1811629

    Figure Lengend Snippet: Diagram of NPC1 functioning in HTNV life cycle. HTNV infection triggers cellular cholesterol redistribution, which requires NPC1. Cholesterol extensively accumulated in late-endosome, thereby amplifying the innate immune response, when HTNV infected NPC1 defective cells. Consequently, NPC1 avoids abnormal endosomal cholesterol accumulation to mitigate innate immune response and promote HTNV replication.

    Article Snippet: Wild-type and NPC1 knockout HeLa cells were grown on a six-well plate for 12 h, 10 μM U18666A and HTNV (MOI = 1) were added to the cells, and the cellular cholesterol level was measured using Tissue Total Cholesterol (TC) Content Assay Kit (APPLYGEN) at 48 h post-infection.

    Techniques: Infection