Effects of sweet almond (Prunus amygdalus) suspension on blood biochemical parameters in experimentally induced hyperlipidemic mice.

The present study aimed to examine the effects of sweet almond (Prunus amygdalus) suspension (SAS) on the measurements of blood biochemical parameters in male albino mice, in which hyperlipidemia was induced experimentally.

Seventy male albino mice were divided randomly into seven groups (10 mice/group). The first group was the untreated control group (negative control). The second group comprised hyperlipidemic mice that did not receive SAS treatment (positive control). The other five groups consisted of hyperlipidemic mice that were orally administered five different doses of SAS (285, 571, 857, 1128, and 1428 mg/kg body weight). Hyperlipidemia was induced in mice by adding 1% cholesterol to the diet along with 0.5% H₂O₂ to the drinking water, with ad libitum access to both food and water for 60 consecutive days. Prothrombin time, partial thromboplastin time, clotting time, and platelet count were measured. Serum lipid profile (total cholesterol [TC], triacylglycerol [TAG], low-density lipoprotein cholesterol [LDL-C], very LDL-C [VLDL-C], and high-density lipoprotein cholesterol [HDL-C]) was also determined.

Prothrombin time, partial thromboplastin time, and clotting time significantly increased only in groups treated with SAS, especially at the dosage of 1428 mg/kg compared with the positive control group. Blood platelet count significantly decreased in SAS-treated groups. The serum levels of TC, TAG, LDL-C, and VLDL-C in the SAS-treated groups (857, 1128, and 1428 mg/kg) significantly decreased, whereas the serum level of HDL-C significantly increased compared with that of the positive control group.SAS administered orally at 1428 mg/kg body weight was the dose that most significantly decreased platelet count and serum levels of TC, TAG, LDL-C, and VLDL-C and increased prothrombin time, partial thromboplastin time, and clotting time as well as serum level of HDL-C in experimentally induced hyperlipidemic mice.