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    Hefei Home Sunshine Pharmaceutical Technology Co.,Ltd
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    Hefei Home Sunshine Pharmaceutical Technology Co., Ltd., founded in 2013, is located in Hefei City, China. The company is ISO 9001:2015 certified and mainly engaged in supplying of API (active pharmaceutical ingredients), intermediates and fine chemicals. We regard product quality and credibility as the life of the enterprise.The management team has more than 15 years of experience in the industry and pays close attention to market dynamics. With a keen sense of market smell, we provide our ...
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    History, efficacy and function of Chenodeoxycholic acid
    Chenodeoxycholic acid was isolated in 1924 from goose gall by Adolf Windaus and human gall by Heinrich Wieland.Its complete structural configuation was elucidated by Hans Lettre at the University of Gottingen.   In 1968, William Admirand and Donald Small at Boston University Medical School established that in patients with gallstones their bile was saturated with cholesterol, sometimes even exhibiting microcrystals, whereas this was not the case in normal people.It was then found that biliary levels of cholic acid and chenodeoxycholic acid were lower in patients with cholesterol gallstones than in normal people. Leslie Thistle and John Schoenfield at the Mayo Clinic in Rochester, Minnesota, then administered individual bile salts by mouth for four months and found that chenodeoxycholic acid reduced the amount of cholesterol in the bile.This led to a national collaborative study in the United States, which confirmed the effectiveness of chenodeoxycholic acid in bringing about dissolution of gallstones in selected patients. However, recent developments such as laparoscopic cholecystectomy and endoscopic biliary techniques have curtailed the role of chenodeoxycholic acid and ursodeoxycholic acid in the treatment of cholelithiasis.     Chenodeoxycholic acid is a bile acid synthesized in the liver from cholesterol. henodeoxycholic acid has been used in a study to assess its effects as a long-term replacement therapy for cerebrotendinous xanthomatosis (CTX). It has also been used in a study to investigate its effects on the small-intestinal absorption of bile acids in patients with ileostomies. Chenodeoxycholic acid is the first agent to be introduced into the US market for the treatment of radiolucent gallstones. Large scale clinical trials have demonstrated the safety and efficacy of this agent.     Chenodeoxycholic acid reduces the biliary concentration of cholesterol relative to that of bile acids and phospholipid, reducing the saturation and thus the lithogenicity of the bile. Success rates in dissolving gallstones are in the range of 50-70% within 4-24 months of treatment. Continuation of the drug after stone dissolution may be required to prevent reoccurrence. Chenodeoxycholic acid is the 7α-isomer of ursodeoxycholic acid which was introduced into the European market in 1978.     Chenodeoxycholic acid is a bile acid that induces apoptosis through protein kinase C signaling pathways.It is a major bile acid in many vertebrates, occurring as the N-glycine and/or N-taurine conjugate. With other bile acids, forms mixed micelles with lecithin in bile which solubilize cholesterol and thus facilitates its excretion.Bile acids are essential for solubilization and transport of dietary lipids, are the major products of cholesterol catabolism, and are physiological ligands for farnesoid X receptor (FXR), a nuclear receptor that regulates genes involved in lipid metabolism.They are also inherently cytotoxic, as physiological imbalance contributes to increased oxidative stress. Bile acid-controlled signaling pathways are promising novel targets to treat such metabolic diseases as obesity, type II diabetes, hyperlipidemia, and atherosclerosis.     Chenodeoxycholic acid is widely utilized in therapeutic applications. It is applied in medical therapy to dissolve gallstones. It is employed in the treatment of cerebrotendineous xanthomatosis. It is used to treat constipation and cerebrotendineous xanthomatosis. It acts as a urea receptor in supramolecular chemistry which can contain anions. It is a staining additive commonly used with ruthenium or organic photo-sensitizers in the preparation of staining solutions for dye solar cells.   Chenodeoxycholic Acid is a staining additive commonly used with ruthenium or organic photo-sensitizers in the preparation of staining solutions for Dye Solar Cells. This co-adsorbent will prevent dye aggregation on the semiconductor surface, reducing losses in the solar cell's operation.   Chenodeoxycholic Acid is a white solid added with the dye powder to the solvent while preparing staining solutions. The concentration of co-adsorbent is typically 10 fold the dye concentration.   Chenodeoxycholic acid has been used in a study to assess its effects as a long-term replacement therapy for cerebrotendinous xanthomatosis (CTX).   It has also been used in a study to investigate its effects on the small-intestinal absorption of bile acids in patients with ileostomies. Chenodeoxycholic acid (CDCA) is a hydrophobic primary bile acid that activates nuclear receptors involved in cholesterol metabolism.EC50 concentrations for activation of FXR range from 13-34 μM.In cells, CDCA also binds to bile acid binding proteins (BABP) with a reported stoichiometry of 1:2.CDCA toxicity is linked to increased cellular glutathione levels and increased oxidative stress. Exposure of cells to excess CDCA contributes to liver and intestinal cancers.  
    The efficacy and production methods of UDCA
    Bile promoting drugs can generally be divided into two types: bile promoting agents and liquid enhancing bile promoting agents. The former refers to drugs that can promote bile secretion, while the latter refers to drugs that only increase bile volume but do not increase bile components. The commonly used cholestatic drugs are mainly bile acids. There are sodium cholic acid, dehydrocholic acid, chenodeoxycholic acid, and ursodeoxycholic acid.   Ursodeoxycholic acid is a chemical preparation that separates natural bile acids from bear bile. It is a stereoisomer of chenodeoxycholic acid, and its litholytic effect and therapeutic effect are similar to those of chenodeoxycholic acid, but the treatment course is short and the dosage is small. It combines with taurine in the body and exists in bile as a hydrophilic bile acid, serving as a cholesterol stone solubilizer. It can reduce the secretion of cholesterol by the liver, lower the saturation of cholesterol in bile, promote the secretion of bile acids, increase the solubility of cholesterol in bile, dissolve cholesterol stones, or prevent the formation of stones. It can increase the secretion of bile, relax the sphincter of the bile duct, and have a diuretic effect, which is conducive to the discharge of stones. This product cannot dissolve other types of gallstones. Ursodeoxycholic acid is suitable for treating cholesterol stones, hyperlipidemia, bile secretion disorders, primary biliary cirrhosis, chronic hepatitis, bile reflux gastritis, and preventing acute rejection and reactions of liver transplantation. The stone dissolving effect of this product is slightly weaker than that of chenodeoxycholic acid.     Production method Method 1: Use chenodeoxycholic acid as raw materials Preparation of 3α, 7α-diacetyl cholic acid methyl ester; Take 36ml of anhydrous methanol, and pass through 1g dried hydrogen chloride gas, add bile acid 12g, stir, heat and reflux for 20-30min. After standing for several hours at room temperature when crystals are separated out, freeze, filter, wash with ether, and dry to obtain methyl cholate. Take 2g methyl cholate, add 9.6 mL of benzene, 2.4mL pyridine, 2.4 mL of acetic anhydride, shake for 10-15min, stand for 20h at room temperature, then pour the reaction mixture into 100ml of water, remove the benzene layer, repeatedly wash with distilled water before recycling the solvents. Wash the solid residue with petroleum ether once, and re-crystallize with methanol-aqueous solution to obtain 3α, 7α-diacetyl bile acid methyl ester. Bile acid methyl → → 3α, 7α-diacetyl bile acid methyl ester Preparation of Chenodeoxycholic acid: Take the 1.5 g diacetyl bile acid methyl ester, add 24 mL acetic acid, add potassium chromate solution (Take 0.76g potassium chromate to dissolve it in 1.8ml take in water), heated to 40 °C, perform reaction for 8h, add water 120ml, shaking for some moment, placed 12h, filter, wash with distilled water till neutralization, dry to give 3α, 7α-diacetoxy-12-keto bile acid methyl ester, referred briefly as the 12-ketone. Take 12-15 g 12-ketone, add 150 mL 2-glycol ether, 15 mL 80% hydrazine hydrate solution, and 15 g potassium hydroxide. Heat to 30 °C and reflux for 15h, heat to 195-200 °C, refluxed for 2.5h, heat to 217 °C for some moment of reaction cool to 190 °C, add 0.7ml hydrazine hydrate solution, heat from within 215 °C to 220 °C within 3h, cool, add 600mL distilled water, adjust to pH 3 with 10% sulfuric acid, separate out the crystals, filter, wash with water until neutralization. Add ethyl acetate, dump the aqueous layer, use water to wash the organic layer was washed for 1-2 times, vacuum distillation and obtain 3α, 7α-dihydroxy cholanic acid, namely Chenodeoxycholic acid. 3α, 7α-diacetyl methyl cholate → 3α, 7α-diacetoxy-12-Keto ursodeoxycholic acid methyl ester → 3α, 7α-dihydroxy ursodeoxycholic acid (Chenodeoxycholic acid) Preparation of refined ursodeoxycholic acid; Taken 2 g chenodeoxycholic acid, add 100ml of acetic acid and 20g potassium acetate, shake to dissolve. Add potassium chromate 1.5g (dissolved in 10 mL of water), at room temperature overnight, add water 200ml, separate out the crystals, filter, wash, and dry to obtain 3α-hydroxy-7-keto-ursodeoxycholic acid. Take 4g 3α-hydroxy-7-keto-ursodeoxycholic acid, add 100 mL n-butanol, heat to about 115 °C, gradually add 8 g metal sodium after which, white slurry gradually comes out, keep reaction for 30min, add 120ml water, stir and heat to transparently dissolve. Evaporate the organic layer under reduced pressure; add 500 mL water to the residue, dissolve, and filter. Adjust the pH the filtrate to pH 3 with 10% sulfuric acid which will yield white precipitate, filter, wash till neutralization with water, dry, wash with ethyl acetate, crystallize with diluted ethanol and obtain 3α, 7β-dihydroxycholanic acid, that’s refined ursodeoxycholic acid. Chenodeoxycholic acid [potassium chromate] → 3α-hydroxy-7-keto acid [sodium metal, 115 °C] → 3α, 7β-Keto ursodeoxycholic acid methyl ester (Ursodeoxycholic acid) Method 2: Use pig bile or bile salts as raw material; Use thin layer chromatography to isolate ursodeoxycholic acid from pigs bile or bile salt. Pig bile salt contains free and bound type of UDCA whose content is about 30%; pig bile contains bound UDCA whose content is about 0.6%.
    A large-scale study found that every bite of pork, beef, and mutton may increase the risk of cancer.
      The results showed that regular consumption of red meat and processed meat increases the risk of colorectal cancer. The study also identified two genes, HAS2 and SMAD7, which can change the level of cancer risk based on the consumption level of red or processed meat. Recently, researchers from the Keck School of Medicine at the University of Southern California published a research paper entitled "Genome-Wide Gene–Environment Interaction Analyses to Understand the Relationship between Red Meat and Processed Meat Intake and Colorectal Cancer Risk" in the journal "Cancer Epidemiology, Biomarkers & Prevention".   This large-scale study shows that regular consumption of red meat and processed meat increases the risk of colorectal cancer. People with higher intake of red meat and processed meat have a 30% and 40% increased risk of colorectal cancer, respectively.   In addition, the study also identified two genes, HAS2 and SMAD7, which can change cancer risk levels based on the consumption level of red or processed meat.   In this study, researchers analyzed data from 27 European colorectal cancer risk studies, including 29,842 colorectal cancer patients and 39,635 non-cancer patients. Participant intake of red and processed meat was collected through dietary questionnaires, and genetic data was analyzed to explore the association between red and processed meat intake and colorectal cancer.   The researchers divided the participants into four groups based on their intake of red meat (beef, pork, and lamb) and processed meat (bacon, sausage, luncheon meat, and hot dogs).   The analysis found that compared with the group with the lowest intake of red meat, the risk of colorectal cancer in the group with the highest intake of red meat increased by 30%; compared with the group with the lowest intake of processed meat, the risk of colorectal cancer in the group with the highest intake of processed meat increased by 40%. Next, the researchers analyzed the genetic data to determine whether there was a genetic variant that could alter the risk of colorectal cancer in people who eat more red meat.   Researchers have discovered two genes, HAS2 and SMAD7, that change cancer risk levels based on red or processed meat consumption levels.   For HAS2 gene, about 66% of the population carries HAS2 gene variants, and compared with the lowest red meat intake group, the highest red meat intake group has a 38% increased risk of colorectal cancer. For the SMAD7 gene, about 74% of the population carries two copies of the SMAD7 gene variant. For people with two copies of the variant, compared to those with the lowest intake of red meat, those with the highest intake of red meat have an 18% increased risk of developing colorectal cancer. Individuals with only one copy of the most common variant or two copies of less common variants have significantly higher cancer risks, at 35% and 46%, respectively. Researchers said that this finding indicates that different genetic variations may lead to different risks of colorectal cancer in individuals who consume red meat, and reveals why red meat and processed meat increase the risk of colorectal cancer.   However, the researchers emphasized that the current study did not prove a causal relationship between these genetic variations.   In short, the results suggest that regular consumption of red and processed meat increases the risk of colorectal cancer. The study also identified two genes, HAS2 and SMAD7, which change cancer risk levels based on the consumption level of red or processed meat.

    2024

    03/18

    A healthier diet can help slow down aging and reduce the risk of dementia
      The MIND diet is a well-known healthy eating pattern that combines the Mediterranean diet with a diet that reduces the risk of high blood pressure.   Recently, Yian Gu, Daniel Belsky and others from Columbia University published a research paper entitled "Diet, Pace of Biological Aging, and Risk of Dementia in the Framingham Heart Study" in the journal Annals of Neurology.   The study found that a healthy diet slows down the rate of biological aging and is associated with a reduced risk of dementia and death. The slowed biological aging rate plays a partial mediating role in the association between a healthy diet and a reduced risk of dementia. Monitoring the rate of aging may help prevent dementia.   In the study of dementia, the focus on nutrition is usually on the impact of specific nutrients on the brain, while this study tests the hypothesis that a healthy diet can prevent dementia by slowing down the overall biological aging rate of the body.   In this study, the research team used data from the second cohort of the Framingham Heart Study, which began in 1971. Participants were aged 60 years or older, had no dementia, and recorded dietary, epigenetic, and follow-up data. They conducted 9 follow-ups approximately every 4-7 years. During each follow-up, data collection included physical examination, lifestyle-related questionnaires, blood sampling, and neurocognitive testing starting in 1991.   Of the 1,644 participants included in the analysis, 140 developed dementia and 471 died during the 14-year follow-up period. To assess their aging rate, the research team used an epigenetic clock, DunedinPACE, to evaluate the rate of decline in a person's body as they age through epigenetics.   Healthy diet can prevent dementia, but the protective mechanism is not clear. Previous studies have linked diet and dementia risk to accelerated biological aging. This study tested the hypothesis that multisystem biological aging is a mechanism of diet-disease association. The study determined that higher adherence to the MIND diet slowed the rate of aging as assessed by the Dunedin PACE and reduced the risk of dementia and death. In addition, in the mediation effect analysis, the slowed Dunedin PACE accounted for 27% of the diet-disease association and 57% of the diet-mortality association.   The MIND diet is a well-known healthy eating pattern that combines the Mediterranean diet with a diet that reduces the risk of high blood pressure.   Overall, the results of this study suggest that the slowing of aging speed plays a partial mediating role in the relationship between a healthy diet and a reduced risk of dementia, and monitoring the aging speed may help prevent dementia. However, a large part of the association between diet and dementia remains unexplained, possibly reflecting a direct link between diet and brain aging that does not overlap with other organ systems. Therefore, further investigation of brain-specific mechanisms is needed in well-designed mediating studies.

    2024

    03/20

    Latest research: 7 hours of sleep per day is the best "maintenance product", too much/little sleep time will accelerate aging
    On the morning of March 16, the Chinese Sleep Research Association announced the annual theme of World Sleep Day in Beijing, "healthy sleep for all". The "2023 White Paper on Chinese Residents' Sleep" released at the meeting showed that the overall sleep quality of Chinese residents is poor, with an average sleep time of 6.75 hours after midnight and an average number of 1.4 awakenings. This is far from the ideal sleep duration and quality. In the field of medicine and health, "phenotypic age" , which is often used as a predictor of various diseases and a biomarker for evaluating aging, refers to a person's physiological age, determined by their physical characteristics and functions rather than their actual age. Research shows that age based biomarkers can be used as reliable indicators for individuals suffering from certain health diseases, such as cardiovascular disease, type II diabetes, nervous system diseases and other chronic disease phenotypes, which can provide more accurate information than actual age or single markers (such as telomere). Although these studies provide some evidence for the relationship between sleep and age-related phenotypic changes, more research is still needed to fully understand this relationship. A study conducted by the Tsinghua University team You et al. analyzed the sleep patterns of 48,762 American adults and the phenotypic age reflected by multiple biomarkers, and found an interesting inverted U-shaped relationship: 7 hours of sleep per day is the optimal "care product" for the human body, and too little or too much sleep time will accelerate the increase of phenotypic age. In addition, this study cleverly incorporated exercise into the scope of discussion, revealing the subtle but crucial relationship between exercise and sleep. According to the data from NHANES, the research team investigated the trend of sleep duration and the relationship between sleep duration and phenotypic age. In different annual cycles, most people's sleep duration is 6-9 hours. Moreover, since the 2015-2016 cycle, the proportion of short sleep and very short sleep has shown a downward trend, while the proportion of long sleep has shown an upward trend. When the researchers used the crude model and Model 1 to evaluate sleep duration as a continuous variable, they found no significant correlation between it and phenotypic age. However, in the fully adjusted model, there was a significant correlation between continuous sleep duration and phenotypic age (Model 2, p=0.031). Compared with the normal sleep group, short sleep duration was positively correlated with phenotypic age in the crude model and model 1 (crude model, p=0.050; model 1, p

    2024

    03/21

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