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total cholesterol kit  (Nanjing Jiancheng Bioengineering Research Institute Co Ltd)

 
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    Nanjing Jiancheng Bioengineering Research Institute Co Ltd total cholesterol kit
    Total Cholesterol Kit, supplied by Nanjing Jiancheng Bioengineering Research Institute Co Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/total+cholesterol+kit/cholesterol+serum+total/pmc13137179-206-14-23
    Average 86 stars, based on 1 article reviews
    total cholesterol kit - by Bioz Stars, 2026-10
    86/100 stars

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    other:

    Article Title: Structure, physicochemical properties, and hypolipidemic activity of soluble dietary fiber obtained from button mushroom ( Agaricus bisporus )
    Article Snippet: A total cholesterol (TC) kit and triglyceride (TG) kit (Nanjing Jiancheng Co., Ltd., Nanjing, China) were employed to measure the TC and TG contents in the supernatant of the samples, respectively ( ).

    Article Title: Characterization and efficacy of α-glucosidase inhibitory peptides from enzymatically hydrolyzed Peanut meal
    Article Snippet: Natural substances with α-glucosidase inhibitory activity have emerged as promising agents for the effective treatment of diabetes.. In this study, peanut meal (PM) was enzymatically hydrolyzed using three proteases and fractionated by ultrafiltration.. Among the resulting fractions, peanut peptide (PEP) in the 3 kDa–500 Da range demonstrated superior α-glucosidase inhibitory activity (69.5%), peptide yield (85.75%), and peptide content (1.55±0.05 mg/mL).

    Article Title: Co-microencapsulation of Lactobacillus paracasei and Inonotus obliquus polysaccharide in alginate system: physicochemical and functional properties
    Article Snippet: In this study, sodium alginate (SA) was used as shell material, and Lactobacillus paracasei JY062/Inonotus obliquus polysaccharide (IOP) were used as core material (JY062-IOP/SA).. The microcapsules were prepared by polymer gel technology and analyzed by SEM, FTIR, TGA and XRD.. The results exhibited that the embedding rate of JY062-IOP/SA microcapsules increased to 89.21 % compared with JY062/SA control group (84.22 %).

    Article Title: Sodium butyrate attenuates lipid metabolism disorder via improving mitochondrial function and activating autophagy in LMH cells.
    Article Snippet: The activities or contents of total cholesterol (TC), TG, superoxide dismutase (SOD) and malondialdehyde (MDA) were measured according to the respective kit instruction manuals (Nanjing Jiancheng Bioengineering Institute, Nanjing, China).

    Article Title: Identification of Foxm1 as a critical regulator for metabolic dysfunction-associated steatotic liver disease by epigenomic and transcriptional profiling
    Article Snippet: Hepatic total cholesterol (TC) and triglyceride (TG) levels were quantified using commercial assay kits (Total Cholesterol Kit, Cat# A111-1-1; Triglyceride Kit, Cat# A110-1-1, Nanjing Jiancheng Bioengineering Institute) according to the manufacturer protocols.

    Article Title: Comparation of brain-targeting chitosan/sodium tripolyphosphate and ovalbumin/sodium carboxymethylcellulose nanoparticles on dihydromyricetin delivery and cognitive impairment in obesity-related Alzheimer's disease.
    Article Snippet: The brain-gut axis plays an important role in regulating cognitive ability in obesity-related Alzheimer's disease (AD).. In this study, we aimed to investigate the correlation between the barrier penetration ability of the DMY nanodelivery system in vivo and the regulation of the gut-brain axis to alleviate cognitive impairment.. Braintargeted peptide (TGN: TGNYKALHPHNG) and DMY loaded chitosan (CS)/sodium tripolyphosphate (TPP) nanoparticles (TGN-DMY-CS/TPP-NPs) and ovalbumin (OVA)/sodium carboxymethylcellulose (CMC) nanoparticles (TGN-DMY-OVA/CMC-NPs) were prepared.

    Mouse Assay:

    Article Title: Fish oil reduces intestinal fat absorption by promoting lacteal junction zippering via GPR120-VEGFR3-MLCK pathway.
    Article Snippet: .. Mice were euthanized by CO2 and subjected to serum analysis for triglycerides, free fatty acids, and total cholesterol using Nanjing Jiancheng Bioengineering Institute kits. ..



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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