Buildup Of Cholesterol Research Articles

Biocompatibility and Haemocompatibility Assessments of RBC with Polymeric Coated Cardiac Stent.

The current investigation was conducted to evaluate the biocompatibility and hemocompatibility of polymeric-coated cardiac stents. Coronary stents are typically small wire mesh tubes that are used to open arteries that are obstructed over time as a result of the buildup of fat, cholesterol, or other materials. A 10 milliliter isolated blood red blood cell was obtained using the Prozeta cobalt chromium coronary stent, which had the following specifications: stent length = 18 mm, strut thickness = 0.065 mm, expansion range = 2.25 mm to 4.00 mm, and burst pressure = 6ATM. Using an R&D coating equipment, polyethylene glycol (PEG) polymers were applied to the coronary stent. Assessments of the polymeric-coated cardiac stent’s biocompatibility and hemocompatibility were conducted using various evaluation criteria. CAD software has been used to help with the stent’s modeling. According to the supplied catalog, the strut’s thickness and width are calculated to be 0.065 mm and its length is 18 mm. The histology of RBC in an isolated sample (polymer coated on stent) found at 2000 Rx was examined using a motic microscope. Using a UV-visible spectrophotometer set to 414 wave length, a 10µg/ml solution of RBC in distilled water was scanned at 200–500 nm to measure the UV absorption maximum. The absorbance was found to be 0.8312 nm. An FTIR analysis of RBC reveals absorptions that include bending and stretching vibrations. Peak Position was discovered at wave numbers 3661.76, 1684.62, 1547.98, 1472.07, 1278.06, and 841.98. Using SEM the surface morphology of RBC was study and it was found the measurements 6.1, 4.2, 3.3, 3.2, 3.1, and 2.2 µm in diameter with standard error 0.548584. It has been determined that PEG-coated material demonstrated significant outcomes that resulted in coronary stent that was both biocompatible and hemocompatible of polymeric-coated cardiac stent, which is a step towards altering the treatment regimen.

Lysosomal cholesterol accumulation in aged astrocytes impairs cholesterol delivery to neurons and can be rescued by cannabinoids.

Cholesterol is crucial for the proper functioning of eukaryotic cells, especially neurons, which rely on cholesterol to maintain their complex structure and facilitate synaptic transmission. However, brain cells are isolated from peripheral cholesterol by the blood-brain barrier and mature neurons primarily uptake the cholesterol synthesized by astrocytes for proper function. This study aimed to investigate the effect of aging on cholesterol trafficking in astrocytes and its delivery to neurons. We found that aged astrocytes accumulated high levels of cholesterol in the lysosomal compartment, and this cholesterol buildup can be attributed to the simultaneous occurrence of two events: decreased levels of the ABCA1 transporter, which impairs ApoE-cholesterol export from astrocytes, and reduced expression of NPC1, which hinders cholesterol release from lysosomes. We show that these two events are accompanied by increased microR-33 in aged astrocytes, which targets ABCA1 and NPC1. In addition, we demonstrate that the microR-33 increase is triggered by oxidative stress, one of the hallmarks of aging. By coculture experiments, we show that cholesterol accumulation in astrocytes impairs the cholesterol delivery from astrocytes to neurons. Remarkably, we found that this altered transport of cholesterol could be alleviated through treatment with endocannabinoids as well as cannabidiol or CBD. Finally, according to data demonstrating that aged astrocytes develop an A1 phenotype, we found that cholesterol buildup is also observed in reactive C3+ astrocytes. Given that reduced neuronal cholesterol affects synaptic plasticity, the ability of cannabinoids to restore cholesterol transport from aged astrocytes to neurons holds significant implications in aging and inflammation.

Heart Attack Prediction using Machine Learning Algorithms

One of the most crucial parts of the human body is the heart. When the heart's blood supply is cut off, a heart attack happens. The most frequent cause of a blockage is the buildup of fats, cholesterol, and other substances inside the coronary arteries that provide blood to the heart (which eventually results in plaque growth). This study sought to identify which anthropometric characteristics had a high likelihood of having an impact on a person having a heart attack in order to design a program for heart attack analysis using machine learning algorithms. The researchers were able to acquire data from a variety of sources to identify the variables that may be used to create the output in order to fulfill the study's objectives. The existing heart attack analysis was reviewed by the researchers. They discovered that the researchers' algorithms were hardly noteworthy. Another ongoing study uses a variety of data mining and machine learning approaches to analyze vast volumes of patient data in an effort to predict heart attacks before they happen, ultimately helping professionals and the healthcare industry. The software for Heart Attack Prediction was created by taking into account various data from previous studies.

Identification of a mechanism promoting mitochondrial sterol accumulation during myocardial ischemia-reperfusion: role of TSPO and STAR.

Hypercholesterolemia is a major risk factor for coronary artery diseases and cardiac ischemic events. Cholesterol per se could also have negative effects on the myocardium, independently from hypercholesterolemia. Previously, we reported that myocardial ischemia-reperfusion induces a deleterious build-up of mitochondrial cholesterol and oxysterols, which is potentiated by hypercholesterolemia and prevented by translocator protein (TSPO) ligands. Here, we studied the mechanism by which sterols accumulate in cardiac mitochondria and promote mitochondrial dysfunction. We performed myocardial ischemia-reperfusion in rats to evaluate mitochondrial function, TSPO, and steroidogenic acute regulatory protein (STAR) levels and the related mitochondrial concentrations of sterols. Rats were treated with the cholesterol synthesis inhibitor pravastatin or the TSPO ligand 4'-chlorodiazepam. We used Tspo deleted rats, which were phenotypically characterized. Inhibition of cholesterol synthesis reduced mitochondrial sterol accumulation and protected mitochondria during myocardial ischemia-reperfusion. We found that cardiac mitochondrial sterol accumulation is the consequence of enhanced influx of cholesterol and not of the inhibition of its mitochondrial metabolism during ischemia-reperfusion. Mitochondrial cholesterol accumulation at reperfusion was related to an increase in mitochondrial STAR but not to changes in TSPO levels. 4'-Chlorodiazepam inhibited this mechanism and prevented mitochondrial sterol accumulation and mitochondrial ischemia-reperfusion injury, underlying the close cooperation between STAR and TSPO. Conversely, Tspo deletion, which did not alter cardiac phenotype, abolished the effects of 4'-chlorodiazepam. This study reveals a novel mitochondrial interaction between TSPO and STAR to promote cholesterol and deleterious sterol mitochondrial accumulation during myocardial ischemia-reperfusion. This interaction regulates mitochondrial homeostasis and plays a key role during mitochondrial injury.

Cholesterol trafficking, lysosomal function, and atherosclerosis.

Despite years of study and major research advances over the past 50 years, atherosclerotic diseases continue to rank as the leading global cause of death. Accumulation of cholesterol within the vascular wall remains the main problem and represents one of the early steps in the development of atherosclerotic lesions. There is a complex relationship between vesicular cholesterol transport and atherosclerosis, and abnormalities in cholesterol trafficking can contribute to the development and progression of the lesions. The dysregulation of vesicular cholesterol transport and lysosomal function fosters the buildup of cholesterol within various intracytoplasmic compartments, including lysosomes and lipid droplets. This, in turn, promotes the hallmark formation of foam cells, a defining feature of early atherosclerosis. Multiple cellular processes, encompassing endocytosis, exocytosis, intracellular trafficking, and autophagy, play crucial roles in influencing foam cell formation and atherosclerotic plaque stability. In this review, we highlight recent advances in the understanding of the intricate mechanisms of vesicular cholesterol transport and its relationship with atherosclerosis and discuss the importance of understanding these mechanisms in developing strategies to prevent or treat this prevalent cardiovascular disease.

Cholesterol redistribution triggered by CYP46A1 gene therapy improves major hallmarks of Niemann-Pick type C disease but is not sufficient to halt neurodegeneration

Cholesterol 24-hydroxylase (CYP46A1) is an exclusively neuronal cytochrome P450 enzyme responsible for converting cholesterol into 24S-hydroxycholesterol, which serves as the primary pathway for eliminating cholesterol in the brain. We and others have shown that increased activity of CYP46A1 leads to reduced levels of cholesterol and has a positive effect on cognition. Therefore, we hypothesized that CYP46A1 could be a potential therapeutic target in Niemann-Pick type C (NPC) disease, a rare and fatal neurodegenerative disorder, characterized by cholesterol accumulation in endolysosomal compartments. Herein, we show that CYP46A1 ectopic expression, in cellular models of NPC and in Npc1tm(I1061T) mice by adeno-associated virus-mediated gene therapy improved NPC disease phenotype. Amelioration in functional, biochemical, molecular and neuropathological hallmarks of NPC disease were characterized. In vivo, CYP46A1 expression partially prevented weight loss and hepatomegaly, corrected the expression levels of genes involved in cholesterol homeostasis, and promoted a redistribution of brain cholesterol accumulated in late endosomes/lysosomes. Moreover, concomitant with the amelioration of cholesterol metabolism dysregulation, CYP46A1 attenuated microgliosis and lysosomal dysfunction in mouse cerebellum, favoring a pro-resolving phenotype. In vivo CYP46A1 ectopic expression improves important features of NPC disease and may represent a valid therapeutic approach to be used concomitantly with other drugs. However, promoting cholesterol redistribution does not appear to be enough to prevent Purkinje neuronal death in the cerebellum. This indicates that cholesterol buildup in neurons might not be the main cause of neurodegeneration in this human lipidosis.

Effect of Regular Exercise on Low-Density Lipoprotein Level

Low-density lipoprotein (LDL) is called bad cholesterol. High LDL level leads to a build-up of cholesterol in arteries, which may elicit heart disease. Therefore, it is necessary to keep under controlled LDL levels for the safety of life. The researchers in this study investigate whether exercise may lead to decreasing the LDL level. A total of sixty undergraduate willing female students, with a mean age (of 22+1 years), were conveniently selected from two populations and divided into two groups: the exercise group (n=30) and the wait-for-list control group (n=30). A total of four hours per day and six days per week of exercise and games were practiced for twelve weeks by the exercise group. The Hitachi 704 analyzer conducted a lipid profile test during pre and post-intervention. The level of LDL was decreased by 32.48% after twelve weeks in the exercise group. It can be explained that the physiological process of fat loss occurs when fats are liberated from adipocytes and other areas into circulation to supply the needed energy during exercise.

G9a and Sirtuin6 epigenetically modulate host cholesterol accumulation to facilitate mycobacterial survival.

Cholesterol derived from the host milieu forms a critical factor for mycobacterial pathogenesis. However, the molecular circuitry co-opted by Mycobacterium tuberculosis (Mtb) to accumulate cholesterol in host cells remains obscure. Here, we report that the coordinated action of WNT-responsive histone modifiers G9a (H3K9 methyltransferase) and SIRT6 (H3K9 deacetylase) orchestrate cholesterol build-up in in vitro and in vivo mouse models of Mtb infection. Mechanistically, G9a, along with SREBP2, drives the expression of cholesterol biosynthesis and uptake genes; while SIRT6 along with G9a represses the genes involved in cholesterol efflux. The accumulated cholesterol in Mtb infected macrophages promotes the expression of antioxidant genes leading to reduced oxidative stress, thereby supporting Mtb survival. In corroboration, loss-of-function of G9a in vitro and pharmacological inhibition in vivo; or utilization of BMDMs derived from Sirt6-/- mice or in vivo infection in haplo-insufficient Sirt6-/+ mice; hampered host cholesterol accumulation and restricted Mtb burden. These findings shed light on the novel roles of G9a and SIRT6 during Mtb infection and highlight the previously unknown contribution of host cholesterol in potentiating anti-oxidative responses for aiding Mtb survival.

Pharmacological interventions for asymptomatic carotid stenosis.

Carotid artery stenosis is narrowing of the carotid arteries. Asymptomatic carotid stenosis is when this narrowing occurs in people without a history or symptoms of this disease. It is caused by atherosclerosis; that is, the build-up of fats, cholesterol, and other substances in and on the artery walls. Atherosclerosis is more likely to occur in people with several risk factors, such as diabetes, hypertension, hyperlipidaemia, and smoking. As this damage can develop without symptoms, the first symptom can be a fatal or disabling stroke, known as ischaemic stroke. Carotid stenosis leading to ischaemic stroke is most common in men older than 70 years. Ischaemic stroke is a worldwide public health problem. To assess the effects of pharmacological interventions for the treatment of asymptomatic carotid stenosis in preventing neurological impairment, ipsilateral major or disabling stroke, death, major bleeding, and other outcomes. We searched the Cochrane Stroke Group trials register, CENTRAL, MEDLINE, Embase, two other databases, and three trials registers from their inception to 9 August 2022. We also checked the reference lists of any relevant systematic reviews identified and contacted specialists in the field for additional references to trials. We included all randomised controlled trials (RCTs), irrespective of publication status and language, comparing a pharmacological intervention to placebo, no treatment, or another pharmacological intervention for asymptomatic carotid stenosis. We used standard Cochrane methodological procedures. Two review authors independently extracted the data and assessed the risk of bias of the trials. A third author resolved disagreements when necessary. We assessed the evidence certainty for key outcomes using GRADE. We included 34 RCTs with 11,571 participants. Data for meta-analysis were available from only 22 studies with 6887 participants. The mean follow-up period was 2.5 years. None of the 34 included studies assessed neurological impairment and quality of life. Antiplatelet agent (acetylsalicylic acid) versus placebo Acetylsalicylic acid (1 study, 372 participants) may result in little to no difference in ipsilateral major or disabling stroke (risk ratio (RR) 1.08, 95% confidence interval (CI) 0.47 to 2.47), stroke-related mortality (RR 1.40, 95% CI 0.54 to 3.59), progression of carotid stenosis (RR 1.16, 95% CI 0.79 to 1.71), and adverse events (RR 0.81, 95% CI 0.41 to 1.59), compared to placebo (all low-certainty evidence). The effect of acetylsalicylic acid on major bleeding is very uncertain (RR 0.98, 95% CI 0.06 to 15.53; very low-certainty evidence). The study did not measure neurological impairment or quality of life. Antihypertensive agents (metoprolol and chlorthalidone) versus placebo The antihypertensive agent, metoprolol, may result in no difference in ipsilateral major or disabling stroke (RR 0.14, 95% CI 0.02 to1.16; 1 study, 793 participants) and stroke-related mortality (RR 0.57, 95% CI 0.17 to 1.94; 1 study, 793 participants) compared to placebo (both low-certainty evidence). However, chlorthalidone may slow the progression of carotid stenosis (RR 0.45, 95% CI 0.23 to 0.91; 1 study, 129 participants; low-certainty evidence) compared to placebo. Neither study measured neurological impairment, major bleeding, adverse events, or quality of life. Anticoagulant agent (warfarin) versus placebo The evidence is very uncertain about the effects of warfarin (1 study, 919 participants) on major bleeding (RR 1.19, 95% CI 0.97 to 1.46; very low-certainty evidence), but it may reduce adverse events (RR 0.89, 95% CI 0.81 to 0.99; low-certainty evidence) compared to placebo. The study did not measure neurological impairment, ipsilateral major or disabling stroke, stroke-related mortality, progression of carotid stenosis, or quality of life. Lipid-lowering agents (atorvastatin, fluvastatin, lovastatin, pravastatin, probucol, and rosuvastatin) versus placebo or no treatment Lipid-lowering agents may result in little to no difference in ipsilateral major or disabling stroke (atorvastatin, lovastatin, pravastatin, and rosuvastatin; RR 0.36, 95% CI 0.09 to 1.53; 5 studies, 2235 participants) stroke-related mortality (lovastatin and pravastatin; RR 0.25, 95% CI 0.03 to 2.29; 2 studies, 1366 participants), and adverse events (fluvastatin, lovastatin, pravastatin, probucol, and rosuvastatin; RR 0.76, 95% CI 0.53 to1.10; 7 studies, 3726 participants) compared to placebo or no treatment (all low-certainty evidence). The studies did not measure neurological impairment, major bleeding, progression of carotid stenosis, or quality of life. Although there is no high-certainty evidence to support pharmacological intervention, this does not mean that pharmacological treatments are ineffective in preventing ischaemic cerebral events, morbidity, and mortality. High-quality RCTs are needed to better inform the best medical treatment that may reduce the burden of carotid stenosis. In the interim, clinicians will have to use other sources of information.

NPC1-dependent alterations in KV2.1–CaV1.2 nanodomains drive neuronal death in models of Niemann-Pick Type C disease

Lysosomes communicate through cholesterol transfer at endoplasmic reticulum (ER) contact sites. At these sites, the Niemann Pick C1 cholesterol transporter (NPC1) facilitates the removal of cholesterol from lysosomes, which is then transferred to the ER for distribution to other cell membranes. Mutations in NPC1 result in cholesterol buildup within lysosomes, leading to Niemann-Pick Type C (NPC) disease, a progressive and fatal neurodegenerative disorder. The molecular mechanisms connecting NPC1 loss to NPC-associated neuropathology remain unknown. Here we show both in vitro and in an animal model of NPC disease that the loss of NPC1 function alters the distribution and activity of voltage-gated calcium channels (CaV). Underlying alterations in calcium channel localization and function are KV2.1 channels whose interactions drive calcium channel clustering to enhance calcium entry and fuel neurotoxic elevations in mitochondrial calcium. Targeted disruption of KV2–CaV interactions rescues aberrant CaV1.2 clustering, elevated mitochondrial calcium, and neurotoxicity in vitro. Our findings provide evidence that NPC is a nanostructural ion channel clustering disease, characterized by altered distribution and activity of ion channels at membrane contacts, which contribute to neurodegeneration.

Candidate SNP Markers Significantly Altering the Affinity of TATA-Binding Protein for the Promoters of Human Hub Genes for Atherogenesis, Atherosclerosis and Atheroprotection.

Atherosclerosis is a systemic disease in which focal lesions in arteries promote the build-up of lipoproteins and cholesterol they are transporting. The development of atheroma (atherogenesis) narrows blood vessels, reduces the blood supply and leads to cardiovascular diseases. According to the World Health Organization (WHO), cardiovascular diseases are the leading cause of death, which has been especially boosted since the COVID-19 pandemic. There is a variety of contributors to atherosclerosis, including lifestyle factors and genetic predisposition. Antioxidant diets and recreational exercises act as atheroprotectors and can retard atherogenesis. The search for molecular markers of atherogenesis and atheroprotection for predictive, preventive and personalized medicine appears to be the most promising direction for the study of atherosclerosis. In this work, we have analyzed 1068 human genes associated with atherogenesis, atherosclerosis and atheroprotection. The hub genes regulating these processes have been found to be the most ancient. In silico analysis of all 5112 SNPs in their promoters has revealed 330 candidate SNP markers, which statistically significantly change the affinity of the TATA-binding protein (TBP) for these promoters. These molecular markers have made us confident that natural selection acts against underexpression of the hub genes for atherogenesis, atherosclerosis and atheroprotection. At the same time, upregulation of the one for atheroprotection promotes human health.

Acute ACAT1/SOAT1 Blockade Increases MAM Cholesterol and Strengthens ER-Mitochondria Connectivity.

Cholesterol is a key component of all mammalian cell membranes. Disruptions in cholesterol metabolism have been observed in the context of various diseases, including neurodegenerative disorders such as Alzheimer's disease (AD). The genetic and pharmacological blockade of acyl-CoA:cholesterol acyltransferase 1/sterol O-acyltransferase 1 (ACAT1/SOAT1), a cholesterol storage enzyme found on the endoplasmic reticulum (ER) and enriched at the mitochondria-associated ER membrane (MAM), has been shown to reduce amyloid pathology and rescue cognitive deficits in mouse models of AD. Additionally, blocking ACAT1/SOAT1 activity stimulates autophagy and lysosomal biogenesis; however, the exact molecular connection between the ACAT1/SOAT1 blockade and these observed benefits remain unknown. Here, using biochemical fractionation techniques, we observe cholesterol accumulation at the MAM which leads to ACAT1/SOAT1 enrichment in this domain. MAM proteomics data suggests that ACAT1/SOAT1 inhibition strengthens the ER-mitochondria connection. Confocal and electron microscopy confirms that ACAT1/SOAT1 inhibition increases the number of ER-mitochondria contact sites and strengthens this connection by shortening the distance between these two organelles. This work demonstrates how directly manipulating local cholesterol levels at the MAM can alter inter-organellar contact sites and suggests that cholesterol buildup at the MAM is the impetus behind the therapeutic benefits of ACAT1/SOAT1 inhibition.

A feasibility study on removing lipid deposition in atherosclerotic plaques with ultrasound-assisted laser ablation

Objective. Atherosclerosis is the buildup of fats, cholesterol, and other substances on the inner walls of arteries. It can affect arteries of heart, brain, arms, legs, pelvis and kidney, resulting in ischemic heart disease, carotid artery disease, peripheral artery disease and chronic kidney disease. Laser-based treatment techniques like laser atherectomy can be used to treat many common atherosclerostic diseases. However, the use of laser-based treatment remains limited due to the high risk of complications and low efficiency in removing atherosclerostic plaques as compared with other treatment methods. In this study, we developed a technology that used high intensity focused ultrasound to assist laser treatment in the removal of the lipid core of atherosclerotic plaques. Approach. The fundamental mechanism to disrupt atherosclerostic plaque was to enhance the mechanical effect of cavitation during laser/ultrasound therapy. To promote cavitation, spatiotemporally synchronized ultrasound bursts of 2% duty cycle at 0.5 MHz and nanosecond laser pulses at 532 nm wavelength were used. Experiments were first performed on pig belly fat samples to titrate ultrasound and laser parameters. Then, experiments were conducted on human plaque samples, where the lipid depositions of the plaques were targeted. Main results. Our results showed that fat tissue could be removed with an ultrasound peak negative pressure (PNP) of 2.45 MPa and a laser radiant exposure as low as 3.2 mJ mm−2. The lipid depositions on the atherosclerostic plaques were removed with laser radiant exposure of 16 mJ mm−2 in synchronizing with an ultrasound PNP of 5.4 MPa. During all the experiments, laser-only and ultrasound-only control treatments at the same energy levels were not effective in removing the lipid. Significance. The results demonstrated that the addition of ultrasound could effectively reduce the needed laser power for atherosclerotic plaque removal, which will potentially improve treatment safety and efficiency of current laser therapies.

Resveratrol Improves the Progression of Osteoarthritis by Regulating the SIRT1-FoxO1 Pathway-Mediated Cholesterol Metabolism.

Osteoarthritis (OA) is considered a metabolic disorder. This study investigated the effect of resveratrol (RES) on cholesterol accumulation in osteoarthritic articular cartilage via the silent information regulator 1 (SIRT1)/forkhead transcription factor (FoxO1) pathway. Interleukin (IL)-1β-treated chondrocytes that mimic OA chondrocytes were used in in vitro experiments. The optimal RES concentration was selected based on the results of chondrocyte proliferation in the Cell Counting Kit-8 assay. Western blotting, immunofluorescence, and reverse transcription-quantitative polymerase chain reaction were performed. For the animal experiments, mice were randomly divided into the RES group (n = 15), medial meniscus destabilization group (n = 15), and sham group (n = 15), and each group received the same dose of RES or saline. Articular cartilage tissue was obtained eight weeks after surgery for relevant histological analysis. Clinical tissue test results suggest that downregulation of the SIRT1/FoxO1 pathway is associated with cholesterol buildup in OA chondrocytes. For the in vitro studies, RES increased the expression of SIRT1 and phosphorylation of FoxO1 in IL-1β-treated chondrocytes, promoted the expression of cholesterol efflux factor liver X receptor alpha (LXRα), and inhibited the expression of cholesterol synthesis-associated factor sterol-regulatory element binding proteins 2 (SREBP2). This reduced IL-1β-induced chondrocytes cholesterol accumulation. SIRT1 inhibition prevented the RES-mediated reduction in cholesterol buildup. Inhibiting FoxO1 but not SIRT1 reduced FoxO1 phosphorylation and increased cholesterol buildup in cultured chondrocytes. Additionally, in vivo experiments have shown that RES can alleviate cholesterol buildup and pathological changes in OA cartilage. Our findings suggest that RES regulates cholesterol buildup in osteoarthritic articular cartilage via the SIRT1/FoxO1 pathway, thereby improving the progression of OA.

The Effect Of Giving Okra Fruit-Infused Water On Recreasing Cholesterol Levels In Hypercholesterolemia Patients In Payan Pabean Sidoarjo Village

Background: In such a modern era, many experiencing society _ an inclined shift _ push for a change in the pattern of a healthy life, where many vote society _ for consuming food ready eat, eating fatty foods, and rarely sport. This _, if done in a manner that keeps going continuously for a period of long time _, will have an impact on the body, one of them i.e., the buildup of cholesterol. Study this aim to identify the influence of giving okra fruit-infused water to decline cholesterol in patients with hypercholesterolemia in hamlets pay customs Methods: The design study is a quasi-experiment with design non-equivalent control group design. With the use taking sample purposive sampling for one month. The population in the study is patients with hypercholesterolemia, with a sample study of as many as 32 people with 16 groups of treatment and 16 groups of control. Data collection using sheet observation and data analysis using paired t-tests. Infused water is given in 1 week. Results: A significance mark p 0.000, more diminutive than 0.05, is appropriate, with the base deciding the paired t-test. Conclusion: it concluded that there is an effect of okra fruit-infused water on a decline in cholesterol in patients with hypercholesterolemia in hamlets Payan Customs Sidoarjo

Solutions to Familial Hypercholestrolemia

FH or (Familial Hypercholesterolemia) is a genetic disease that passes on from one family member to another, and affects about 1/250 people around the world, but is untreated even though it has a high risk with the addition of increasing one's chances of getting coronary heart disease. This disease causes plaques on the sides of blood vessels (over the build-up of cholesterol). There are 4 solutions worth mentioning Lomitapide, Statins, Surgery, and Genetic engineering. Lomitapide is a pill to be taken by mouth and it takes action in the early processes of making triglycerides. Statins are used to reduce the level of LDL Proteins in the Liver. The surgical options are to be used in rare cases as not all situations are the same and may not be for anyone and everyone. The Genetic engineering solution is gonna be used as a therapeutic method that has never been tried before, it may prevent future generation problems.

Molecular Docking Study Reveals α-Santalol from Santalum album Linn. as Promising Inhibitor of CD36 for Atherosclerosis

Atherosclerosis is an inflammatory vascular disease defined by the increasing buildup of cholesterol in the walls of the arteries, and it is a primary contributor to cardiovascular diseases (CVDs). Issues concerning the adverse effects of synthetic treatments have recently resulted in a lack of patient consultations, drug misuse, and, as a result, a disturbance in meticulous disease control. As a result, a new understanding of traditional medicines has recently developed, and much research has been undertaken on such botanicals in an attempt to produce newer naturally based drugs. Santalum album, commonly known as sandalwood is one of the promising botanicals which is rich in α-Santalol. Therefore, the present study aims at exploring the targeting ability of α-Santalol against the protein CD36 which plays a significant part in the development and progression of atherosclerosis. In this research, a computation approach using Autodock4 is carried out which revealed negative binding energy of 9.10Kcal/mol highlighting the potential of α-Santalol for the effective management of cardiovascular diseases like atherosclerosis. However, there is still a need to validate the findings of this research with both, In Vivo and In Vitro studies.

Screening bile salt hydrolase activity of Lactobacillus isolated from Vietnamese human origins

Hypercholesterolemia is a major cause of cholesterol build-up in the coronary arteries, which can subsequently lead to heart disease or atherosclerosis. Cholesterol levels can be lowered by cholesterol-lowering drugs but some of these drugs may have harmful side effects, while supplementation of Lactobacillus has shown the potential to reduce serum cholesterol levels by virtue of bile salt hydrolase (bsh) activity. In this study, Lactobacillus plantarum VFE-04, L. rhamnosus VFE-08, and L. plantarum VFE-14, had been isolated from Vietnamese healthy adults, were able to deconjugate glycodeoxycholate (GDC) on MRS plates and MRS broth supplemented with GDC. In addition, deconjugating activity of L. plantarum VFE-04, L. rhamnosus VFE-08, and L. plantarum VFE-14 were also found in cell-free extract as expressed by amount of glycine that released in the supernatant. Four bsh genes including bsh1, bsh2, bsh3, and bsh4 have been identified by PCR in these strains. In addition, L. plantarum VFE-04, L. rhamnosus VFE-08, and L. plantarum VFE-14 also showed high ability to resist bile salts and low pH. The results of 16S rRNA gene analyses showed that L. plantarum VFE-04, L. rhamnosus VFE-08, and L. plantarum VFE-14 and had high similarity scores with L. plantarum ZZU 23 (100%), L. rhamnosus JCM 1136 (99%) and L. plantarum S7 (98.65%), respectively. This study suggests that L. plantarum VFE-04, L. rhamnosus VFE-08, and L. plantarum VFE-14 have the potential to be explored as probiotics in the management of hypercholesterolaemia in near future.

Protective effect of fish oil targeting hadhaa (3-ketoacyl-CoA thiolase, alpha subunit a and hadhb (3-ketoacyl-CoA thiolase, beta subunit) against high cholesterol diet (HCD) induced atherosclerosis on Zebrafish

Currently a high mortality rate is observed due to heart diseases such as atherosclerosis and myocardial infarction, which are mainly caused due to high cholesterol. More novel drugs are needed to replace the currently available drugs to reduce the side effects. Zebrafish are an effective model for lipid metabolism studies in vertebrates. Because it shares 80% of diseases related genes similarity with humans. Zebrafish (Male) were fed with high cholesterol diet to induce atherosclerosis and the cholesterol levels of the Zebrafish are measured. Further, the m RNA expression of hadhaa and hadhb genes in the liver, intestine, and skeletal muscle of Zebrafish are studied. Finally, the atherosclerotic protective effects of fish oil are studied using fluorescence imaging of EGPF Zebrafish larvae and using nail red staining. In this study, we evaluated the effect of a fish oil-rich diet, dietary lipids reported having anti-obesity effects in animals, or cholesterol build-up in Zebrafish. Zebrafish were fed a high cholesterol diet containing 20% (w/w) fish oil. Zebrafish in the fish oil-fed group has 40% less cholesterol build-up than in the regular diet group. The genes encoding beta oxidases such as hadhaa and hadhb are expressed 2 fold higher in the gut of the fish oil treated group. Thiolase/enoyl coenzyme A-hydrates were 20% higher in the test (fish oil) diet group than in the normal diet (pellets) group (p < 0.05). The expression of the fatty acid synthesis gene (fasn) in the liver was considerably reduced in the fish oil group compared to the normal diet group (p < 0.05). These results show that fish oil may reduce cholesterol accumulation and might be used as an effective tool for anti-atherosclerotic drug development and on functional foods with further research. • In this research article we have discussed the possible effect of fish oil over HCD fed Zebrafish. • We have observed a positive effect on fish oil fed Zebrafish. • We suggest that the fish oil may have ability to reduce cholesterol accumulation and blood cholesterol level reduction. • All fishes subjected to the study are male Zebrafish.

Autophagy is differentially regulated in leukocyte and nonleukocyte foam cells during atherosclerosis

Background and Aims : Atherosclerosis is characterized by an accumulation of foam cells within the arterial wall, resulting from excess cholesterol uptake and buildup of cytosolic lipid droplets (LDs). Autophagy promotes LD clearance by freeing stored cholesterol for efflux, a process that has been shown to be atheroprotective. While the role of autophagy in LD catabolism has been studied in macrophage (Mϕ)-derived foam cells, this has remained unexplored in vascular smooth muscle cell (VSMC)-derived foam cells.