Probiotics combined with atorvastatin administration in the treatment of hyperlipidemia: A randomized, double-blind, placebo-controlled clinical trial.

BACKGROUND: Hyperlipidemia is a common feature of chronic diseases. The aim of this work was designed to assess the role of probiotics (Lactobacillus casei Zhang, Bifidobactetium animalis subsp. lactis V9, and Lactobacillus plantarum P-8) in the treatment of hyperlipidemia. METHODS: Thirty three patients with hyperlipidemia were randomly divided into a probiotic group (n = 18) and a control group (n = 15). The probiotic group was administered probiotics (2 g once daily) and atorvastatin 20 mg (once daily), and the control group was administered a placebo (2 g once daily) and atorvastatin 20 mg (once daily). Serum and fecal samples were gathered for subsequent analyses. RESULTS: Time had a significant effect on the total cholesterol (TC), triglycerides (TG), and low-density lipoprotein-cholesterol (LDL-C) levels in the probiotic and control groups (P < .05). The gut microbial abundance in the probiotic group was markedly higher than that in the control group following 3-month probiotic treatment (P < .05). At the phylum level, probiotics exerted no notable effects on the relative abundance of Firmicutes, Bacteroidetes, and Actinobacteria but elevated that of Tenericutes and reduced Proteobacteria. At the genus level, probiotics increased the relative abundance of Bifidobacterium, Lactobacillus, and Akkermansia, and decreased that of Escherichia, Eggerthella, and Sutterella relative to the control group in months 1, 2, and 3 (P < .05). CONCLUSIONS: Probiotics optimize the gut microbiota structure and decrease the amount of harmful bacteria in patients with hyperlipidemia. Probiotics can influence the composition of gut microorganisms and increase their diversity and abundance in vivo. It is recommended to use probiotics combined with atorvastatin to treat patients with hyperlipidemia.

Diosmetin inhibits apoptosis and activates AMPK-induced autophagy in myocardial damage under hypoxia environment.

Inhibition of hypoxia-induced cardiomyocyte apoptosis is considered as an important treatment method for ischemic heart diseases, but related drugs are still insufficient. The present study aims to explore the protective function and mechanism of the key Chinese medicine monomer diosmetin (DIOS) on the injury of cardiomyocytes induced by hypoxia. Here, AC16 and HCM-a cells were treated with 40 µM of DIOS under hypoxic environment and a hypoxic rat model was built to study the role of DIOS. The viability and autophagy of cardiomyocytes were increased, but the apoptosis of cells was suppressed by 40 µM DIOS, under hypoxic environment. Intriguingly, 10 mM 3-methyladenine, an inhibitor of autophagy, reversed the effect of DIOS on autophagy and apoptosis of the cardiomyocytes under hypoxia. Furthermore, DIOS induced AMP-activated protein kinase (AMPK) activation and Compound C (5 µM), an AMPK inhibitor, attenuated the inhibition of DIOS on the apoptosis of cardiomyocytes under hypoxia environment. In isoprenaline-induced hypoxic rats, it was verified that DIOS inhibited apoptosis, accelerated autophagy, and activated AMPKα pathway in vivo. Our findings indicated that DIOS alleviated hypoxia-induced myocardial apoptosis via inducing the activation of AMPK-induced autophagy. In summary, the study suggested that DIOS inhibited the apoptosis and induced the autophagy of hypoxia-induced cardiomyocytes through AMPK activation.