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Meril Diagnostics kits for total protein
Kits For Total Protein, supplied by Meril Diagnostics, 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/pm36247333-54-8-16
Average 90 stars, based on 1 article reviews
kits for total protein - by Bioz Stars, 2026-10
90/100 stars

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Article Title: Gallic acid reverses ovarian disturbances in mice with letrozole-induced PCOS via modulating Adipo R1 expression
Article Snippet: Using readily accessible kits, total cholesterol (TC), triglycerides (TG), and high density lipoprotein (HDL) was colorimetrically assessed (Meril Diagnostics).

Article Title: Vitamin C mitigates hematological and biochemical alterations caused by di(2-ethylhexyl) phthalate toxicity in female albino mice, Mus musculus .
Article Snippet: The kits for glucose, cholesterol, triglycerides, and total protein were obtained from the Elab science and Meril Diagnostics.

Article Title: Diacerein mitigates endocrine and cardio-metabolic disruptions in experimental PCOS mice model by modulating AdipoR1/ PON 1.
Article Snippet: Using established colorimetric techniques and reagents from Meril Diagnostics (Gujrat, India) triglyceride (TG), total cholesterol (TC), and high-density lipoprotein-cholesterol (HDL-C) were determined in the serum, heart, and ovarian tissue homogenates.

Article Title: Ameliorative effects of quercetin on endocrine and metabolic abnormalities associated with experimentally induced polycystic ovary syndrome in mice
Article Snippet: The ubiquitous endocrine condition known as the polycystic ovarian syndrome (PCOS) has an effect on the health of many women around the world.. Since the specific aetiology is unknown, the diagnostic criteria are currently insufficient, which contributes to the underdiagnosis and under treatment of PCOS in many women.. Eighteen adult Parkes strain mice (age: 4–5 weeks) having a body weight of 18–21 g were separated into three groups at random with 6 animals each as follows: group I, serving the control, received water and a normal chow diet for 45 days; group II received oral gavage administration of letrozole (LETZ) (6 mg/kg bw) which was dissolved in 0.9% NaCl solution for 21 days for the induction of PCOS; group III received oral gavage administration of LETZ (6 mg/kg) for 3 weeks followed by the administration of quercetin (QUER) (125 mg/kg bw orally daily) for 45 days.

Article Title: Effect of quercetin on steroidogenesis and folliculogenesis in ovary of mice with experimentally-induced polycystic ovarian syndrome.
Article Snippet: Using easily accessible kits, triglycerides (TG) and total cholesterol (TC) were colorimetrically measured (Meril Diagnostics, Gujrat, India).

Article Title: Role of diacerein on steroidogenesis and folliculogenesis related genes in ovary of letrozole-induced PCOS mice.
Article Snippet: Polycystic ovary syndrome (PCOS), an intricate and multifaceted metabolic-endocrine disorder that typically affects 6–20% of women of reproductive age and accounts for 70–80% of all occurrences of infertility globally.. In this study we focussed on the effect of diacerein (DIC) on steroidogenesis and follicle development in addition to the basic metabolic and endocrine problems which are associated with PCOS.. Eighteen mature female parkes strain mice were separated into three groups at random with 6 animals in a group as follows: Group I, received water and normal diet for 66 days; group II received letrozole (LETZ) (6 mg/kg bw) for the induction of PCOS; Group III received LETZ (6 mg/kg) for 3 weeks followed by the administration of DIC (35 mg/kg) for 45 days.



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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