Search

Background: The discovery of traditional plants' medicinal and nutritional properties has opened up new avenues for developing pharmaceutical and dietary strategies to prevent atherosclerosis. However, the effect of the antioxidant Dendrobium officinale polysaccharide (DOP) on atherosclerosis is still not elucidated. Purpose: This study aims to investigate the inhibitory effect and the potential mechanism of DOP on high-fat diet-induced atherosclerosis in Apolipoprotein E knockout (ApoE−/−) mice. Study design and methods: The identification of DOP was measured by high-performance gel permeation chromatography (HPLC) and Fourier transform infrared spectroscopy (FTIR). We used high-fat diet (HFD)-induced atherosclerosis in ApoE−/− mice as an animal model. In the DOP intervention stage, the DOP group was treated by gavage with 200 μL of 200 mg/kg DOP at regular times each day and continued for eight weeks. We detected changes in serum lipid profiles, inflammatory factors, anti-inflammatory factors, and antioxidant capacity to investigate the effect of the DOP on host metabolism. We also determined microbial composition using 16S rRNA gene sequencing to investigate whether the DOP could improve the structure of the gut microbiota in atherosclerotic mice. Results: DOP effectively inhibited histopathological deterioration in atherosclerotic mice and significantly reduced serum lipid levels, inflammatory factors, and malondialdehyde (F/B) production. Additionally, the levels of anti-inflammatory factors and the activity of antioxidant enzymes, including superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), were significantly increased after DOP intervention. Furthermore, we found that DOP restructures the gut microbiota composition by decreasing the Firmicutes/Bacteroidota (F/B) ratio. The Spearman's correlation analysis indicated that serum lipid profiles, antioxidant activity, and pro-/anti-inflammatory factors were associated with Firmicutes, Bacteroidota, Allobaculum, and Coriobacteriaceae_UCG-002. Conclusions: This study suggests that DOP has the potential to be developed as a food prebiotic for the treatment of atherosclerosis in the future. [ABSTRACT FROM AUTHOR]

Mutations of the FBN1 gene lead to Marfan syndrome (MFS), which is an autosomal dominant connective tissue disorder featured by thoracic aortic aneurysm risk. There is currently no effective treatment for MFS. Here, we studied the role of mitochondrial dysfunction in the phenotypic transformation of human smooth muscle cells (SMCs) and whether a mitochondrial boosting strategy can be a potential treatment. We knocked down FBN1 in SMCs to create an MFS cell model and used rotenone to induce mitochondrial dysfunction. Furthermore, we incubated the shFBN1 SMCs with Coenzyme Q10 (CoQ10) to assess whether restoring mitochondrial function can reverse the phenotypic transformation. The results showed that shFBN1 SMCs had decreased TFAM (mitochondrial transcription factor A), mtDNA levels and mitochondrial mass, lost their contractile capacity and had increased synthetic phenotype markers. Inhibiting the mitochondrial function of SMCs can decrease the expression of contractile markers and increase the expression of synthetic genes. Imposing mitochondrial stress causes a double-hit effect on the TFAM level, oxidative phosphorylation and phenotypic transformation of FBN1-knockdown SMCs while restoring mitochondrial metabolism with CoQ10 can rapidly reverse the synthetic phenotype. Our results suggest that mitochondria function is a potential therapeutic target for the phenotypic transformation of SMCs in MFS. [ABSTRACT FROM AUTHOR]

Okra is a new type of healthy vegetable and belongs to the homology of medicine and food in traditional Chinese medicine. It is rich in nutrients and active ingredients (i.e. dietary fiber, vitamins, oils, polysaccharides, polyphenols), which makes it to have antioxidant, anti-inflammatory, hypoglycemic, hypolipidemic and other functions. This paper reviews various ingredients in okra, their health benefits and their mechanism of action; also pays attention to the influence of different processing methods on the quality of okra. [ABSTRACT FROM AUTHOR]

Yu Liu, Zhengyang Zhang, Yongting Luo, Peng An, Jingyi Qi, Xu Zhang, Shuaishuai Zhou, Yongzhi Li, Chong Xu, Junjie Luo, and Jiaping Wang. Product of traditional Chinese medicine longgui yangxinwan protects the human body from altitude sickness damage by reducing oxidative stress and preventing mitochondrial dysfunction. High Alt Med Biol. 00:00-00, 2024. Background: Plateau reaction, caused by high-altitude exposure, results in symptoms like headaches, dyspnea, palpitations, fatigue, shortness of breath, and insomnia due to reduced oxygen levels. Mitochondria are crucial for high-altitude acclimatization as they regulate oxygen metabolism and cellular energy, reducing oxidative stress and maintaining bodily functions. Methods: The study participants were randomly divided into placebo group, Rhodiola group and longgui yangxinwan (Original name: taikong yangxinwan) group, with 20 people in each group. Three groups of subjects were sampled at three time points (PI: pre-intervention; P-D1: high-altitude day 1; P-D7: high-altitude day 7), and blood pressure, blood oxygen, heart rate, hemoglobin, and red blood cell count were measured. The ATP content, mitochondrial DNA copy number, expression of mitochondria-related genes, reactive oxygen species (ROS), glutathione peroxidase (GSH-PX) and malondialdehyde (MDA) levels, and mitochondrial morphology were measured in blood at each time point. Results: Our study results demonstrate that longgui yangxinwan keeps the selected human physiological indicators stable and prevents mitochondrial dysfunction in the high altitude. Mechanically, longgui yangxinwan decreases the level of ROS in human serum, whereas increases the activity of the antioxidant enzyme GSH-PX. At high-altitude day 1 (P-D1) and high-altitude day 7 (P-D7), ROS in the placebo group were 1.5 and 2.2-fold higher than those of the longgui yangxinwan group, respectively. In addition, longgui yangxinwan enhances ATP production capacity, restores the levels of mitochondrial respiratory chain complexes, and effectively maintains mitochondrial morphology and integrity. At P-D1 and P-D7, the ATP levels in the longgui yangxinwan group were 19-fold and 26-fold higher than those in the placebo group, respectively. Conclusions: Our study highlights longgui yangxinwan as a potential drug for protecting humans from high-altitude damage by reducing oxidative stress and preventing mitochondrial dysfunction.