In vivo evaluation of hypolipidemic and antioxidative effect of 'Ajwa' (Phoenix dactylifera L.) date seed-extract in high-fat diet-induced hyperlipidemic rat model.

In the present study, we investigated the hypolipidemic and hepatoprotective potential of the commercially available crushed Ajwa date seed-extract on the toxicity caused by the atorvastatin in high-fat diet (HFD)-induced hyperlipidemic rats. Male albino rats were divided into two main groups, Group I (normal control) and Group II (HFD); Group II was further divided into four subgroups: Group IIa (HFD control), Group IIb (Atorvastatin: A10)-6 rats were administered with 10 mg/kg atorvastatin daily for 30 days, Group IIc (Ajwa seed extract: AJ)-6 rats were given 1000 mg/kg Ajwa seed extract daily for 30 days, Group IId (AJ + A10)-6 rats were given Ajwa seed extract 1000 mg/kg and Atorvastatin 10 mg/kg daily for 30 days. The data obtained suggested that Ajwa seed extract lowered the serum cholesterol level in HFD rats and demonstrated the hepatoprotective effect in combination with atorvastatin by reducing the levels of ALT and AST. In conclusion, it protected the tissues from the detrimental effects of hyperglycemia and enhanced antioxidant activity. Furthermore, the dose-limiting toxicity of atorvastatin may be reduced if the Ajwa seed extract is incorporated in the current treatment regimens to treat hyperlipidemia in hypercholesteremic individuals.

Atorvastatin Treatment Modulates the Gut Microbiota of the Hypercholesterolemic Patients.

Hypercholesterolemia is one of the most important risk factors for development of cardiovascular diseases. The composition of gut microbiota (total microbes residing in the gut) impacts on cholesterol and lipid metabolism. On the contrary, alterations in gut microbiota in response to hypercholesterolemia or drug treatment with atorvastatin (a cholesterol-lowering agent) are rarely investigated. We performed 16S rDNA amplicon sequencing to evaluate the gut bacterial community of 15 untreated hypercholesterolemic patients (HP) and 27 atorvastatin-treated hypercholesterolemic patients (At-HP) and compared with 19 healthy subjects (HS). In total, 18 different phyla were identified in the study groups. An increase in relative abundance of Proteobacteria was observed in the HP group compared with At-HP and HS groups. The atherosclerosis-associated genus Collinsella was found at relatively higher abundance in the HP group. The anti-inflammation-associated bacteria (Faecalibacterium prausnitzii, Akkermansia muciniphila, and genus Oscillospira) were found in greater abundance, and proinflammatory species Desulfovibrio sp. was observed at decreased abundance in the drug-treated HP group compared with the untreated HP group. Relative abundances of the Bilophila wadsworthia and Bifidobacterium bifidum (bile acid-associated species) were decreased in the At-HP group. The At-HP and HS clustered separately from HP in the principal coordinate analysis. Decreased bacterial diversity was observed in the atorvastatin-treated group. In conclusion, these data suggest that atorvastatin treatment of patients with hypercholesterolemia may selectively restore the relative abundance of several dominant and functionally important taxa that were disrupted in the HP. Further studies are required to investigate the putative modifying effects of hypocholesterolemic drugs on functionality of gut microbiota, and the potential downstream effects on human health.

Effect of atorvastatin on the gut microbiota of high fat diet-induced hypercholesterolemic rats.

The aim of the present study was to investigate alterations in gut microbiota associated with hypercholesterolemia and treatment with atorvastatin, a commonly prescribed cholesterol-lowering drug. In this study, seven experimental groups of rats were developed based on diets [high-fat diet (HFD) and normal chow diet (NCD)] and various doses of atorvastatin in HFD and NCD groups. 16S rRNA amplicon sequencing was used to analyze the gut microbiota. Atorvastatin significantly reduced the cholesterol level in treated rats. Bacterial diversity was decreased in the drug-treated NCD group compared to the NCD control, but atorvastatin-treated HFD groups showed a relative increase in biodiversity compared to HFD control group. Atorvastatin promoted the relative abundance of Proteobacteria and reduced the abundance of Firmicutes in drug-treated HFD groups. Among the dominant taxa in the drug-treated HFD groups, Oscillospira, Parabacteroides, Ruminococcus, unclassified CF231, YRC22 (Paraprevotellaceae), and SMB53 (Clostridiaceae) showed reversion in population distribution toward NCD group relative to HFD group. Drug-treated HFD and NCD groups both showed an increased relative abundance of Helicobacter. Overall, bacterial community composition was altered, and diversity of gut microbiota increased with atorvastatin treatment in HFD group. Reversion in relative abundance of specific dominant taxa was observed with drug treatment to HFD rats.