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Chunghyul-dan has inhibitory effects on HMG-CoA reductase and pancreatic lipase. We investigated whether Chunghyul-dan has therapeutic effects on humans with hypercholesterolemia. This study was a case-control, open-labeled clinical study. Subjects were treated with Chunghyul-dan (600 mg/day) or Atorvastatin (10 mg/day) for 8 weeks. Serum lipids were checked at baseline after 4 and 8 weeks of medication. While, Chunghyul-dan showed significant lipid-lowering effects, it was less effective than Atorvastatin. In comparison with the histological controls, Chunghyul-dan's effects were superior to placebo. On safety assessment, there was no adverse effect with the use of Chunghyul-dan in hepatic or renal toxicity. In conclusion, we suggest that Chunghyul-dan is a useful herbal medicine for hypercholesterolemia.

We observed that curry leaf (Murraya koenigii) extract possesses the property to decrease blood cholesterol and blood glucose levels in diabetic ob/ob mice. Mice received daily intraperitoneal injections of 80 mg/kg curry leaf extract for 10 consecutive days. The extract significantly decreased blood cholesterol level from 277.6 ± 16.6 mg/d (day 0) to 182.0 ± 15.3 mg/d (day 10, p < 0.01 compared with the change in vehicle group). The extract also significantly decreased blood glucose level from 387.0 ± 15.6 mg/dl (day 0) to 214.0 ± 26.6 mg/dl (day 10, p < 0.01). In addition, body weight was reduced after extract treatment. Our data suggest that curry leaf may be proved to be of clinical importance in improving the management of high cholesterol level and type 2 diabetes.

The roots of Cistanche (C.) tubulosa (Orobanchaceae), a parasitic plant that grows in the Taklamakan desert, are traditionally used as medicines and foods in China. We prepared aqueous ethanol extract (CTE) from the roots of C. tubulosa and its hypocholesterolemic effect was evaluated. Using gene chip and RT-PCR analysis of the livers of mice given CTE (400 mg/kg) for 14 days, we found mRNA expression of molecules related to cholesterol transport [apolipoprotein B and very low density lipoprotein (VLDL) receptor] and metabolism [cytochrome P450 side chain cleave (SCC) and steroid 5α-reductase 2] were up-regulated. The administration of CTE (400 mg/kg) for 14 days significantly suppressed serum cholesterol elevation in high cholesterol diet-fed mice. The mRNA expressions of VLDL receptor and cytochrome P450 SCC were significantly enhanced. In addition, acteoside, a major constituent of CTE, was found to enhance the mRNA expressions of apolipoprotein B, VLDL receptor, and cytochrome P450 SCC in HepG2 hepatocytes. These results suggest that CTE affects the mRNA expressions of molecules related to cholesterol transport and metabolism and exhibits hypocholesterolemic activity in diet-induced hypercholesterolemia mice. Acteoside was involved in the hypocholesterolemic activity of CTE.

Background: Cardiovascular diseases have long been studied to identify their causal factors and counteract them effectively. Atherosclerosis, an inflammatory process of the blood vessel wall, is a common cardiovascular disease. Among the many well-known risk factors, hypercholesterolemia is undoubtedly a significant condition for atherosclerotic plaque formation and is linked to atherosclerosis on many levels, i.e. cell interactions, cytokines levels, diet, and lifestyle. Current studies suggest that controlling balance between proinflammatory (M1) and anti-inflammatory (M2) types of macrophages may be used for patient condition improvement and necrotic core reduction. Methods: This study considered the effects of hypercholesterolemia on the population dynamics of macrophages (M0, M1, M2, foam cells) in atherosclerotic plaque. A mathematical model using a matrix approach to population dynamics was proposed and tested in various scenarios. In order to check model sensitivity and variability associated with error propagation, the uncertainty analysis was performed based on the Monte Carlo approach. Results: Simulations of macrophage population dynamics provided the assessment of necrotic core development and plaque instability. Excess lipid levels emerged as the most critical factor for necrotic core development. However, plaque growth can be significantly slowed if macrophages and foam cells can maintain proper lipid levels. This balance may be disrupted by proinflammatory lipids that eventually will increase plaque size, what is also reflected by M1/M2 dynamics. Conclusion: Hypercholesterolemia accelerates atherosclerosis development, leading to earlier cardiovascular incidents. In silico results suggest that reducing lipid intake and portion of proinflammatory lipids is crucial to slowing plaque development and reducing rupture risk, all of which requires preserving fragile M1/M2 balance. Targeting the inflammatory microenvironment and macrophage polarization represents a promising approach for atherosclerosis management.