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total plasma cholesterol (cho  (BioSino Inc)

 
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    Structured Review

    BioSino Inc total plasma cholesterol (cho
    Total Plasma Cholesterol (Cho, supplied by BioSino Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/total+cholesterol+kit/total+cholesterol++tc++kit/pmc10576099-539-0-4
    Average 90 stars, based on 1 article reviews
    total plasma cholesterol (cho - by Bioz Stars, 2026-11
    90/100 stars

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    Related Articles

    other:

    Article Title: Combination of mangiferin and T0901317 targeting autophagy promotes cholesterol efflux from macrophage foam cell in atherosclerosis
    Article Snippet: TG and total cholesterol (TC) assay kits were purchased from BioSino Bio-Technology and Science Inc. (Beijing, China).

    Article Title: Combination of mangiferin and T0901317 targeting autophagy promotes cholesterol efflux from macrophage foam cell in atherosclerosis.
    Article Snippet: TG and total cholesterol (TC) assay kits were purchased from BioSino Bio-Technology and Science Inc. (Beijing, China).

    Article Title: Endothelial discoidin domain receptor 1 senses flow to modulate YAP activation
    Article Snippet: Total plasma cholesterol (CHO) (BioSino, 000180), triglycerides (TGs) (BioSino, 000220), low-density lipoprotein cholesterol (LDL-C) (BioSino, 020245), and high-density lipoprotein cholesterol (HDL-C) levels (BioSino, 020235) were determined using assay kits.

    Article Title: Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice
    Article Snippet: The commercial kits of total cholesterol (TC), TG, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were purchased from Biosino Bio-Technology and Science Inc. (Beijing, China).

    Article Title: Endothelial discoidin domain receptor 1 senses flow to modulate YAP activation.
    Article Snippet: Total plasma cholesterol (CHO) (BioSino, 000180), triglycerides (TGs) (BioSino, 000220), low-density lipoprotein cholesterol (LDL-C) (BioSino, 020245), and high-density lipoprotein cholesterol (HDL-C) levels (BioSino, 020235) were determined using assay kits.

    Article Title: Total saponins from quinoa bran alleviate high-fat diet-induced obesity and systemic inflammation via regulation of gut microbiota in rats.
    Article Snippet: The levels of TG, total cholesterol (TC), HDL- C, and LDL- C in serum samples were assayed according to the manufacturer's instructions (BioSino Bio- technology and Science, Inc., Beijing, China).

    Clinical Proteomics:

    Article Title: Annexin A1 binds PDZ and LIM domain 7 to inhibit adipogenesis and prevent obesity
    Article Snippet: .. Plasma cholesterol (100000180; BioSino), triglycerides (TG) (100000220; BioSino), and glucose (100000240; BioSino) were measured using enzymatic methods. .. Free glycerol content (E1002; Applygen, Beijing, China) and the levels of non-esterified fatty acid (NEFA) were measured by a colorimetric assay (294-63601; Wako Chemical, Richmond, VA).



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    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