Objective:

2

To observe the changes of dysfunctional high density lipoprotein cholesterol (dyHDL) and the intervention effect of Xiangsha Liu Junzitang in rats with spleen deficiency and hyperlipidemia

and reveal the effect and mechanism of Xiangsha Liu Junzitang on dyHDL in rats with spleen-deficiency hyperlipidemia.

Method:

2

Seventy-five SPF SD rats were randomly divided into normal group

high fat group

spleen deficiency and high fat group

Xiangsha Liu Junzitang low and high dose groups (5.67

11.34 g·kg

-1

). In the spleen deficiency and high fat group

as well as Xiangsha Liu Junzitang low and high dose groups

composite method of improper diet and exhaustive swimming was used for 15 days for modeling. After modeling for 15 days

normal group was fed with basic diet

while the high-fat group

spleen-deficiency and high-fat group

the Xiangsha Liu Junzitang low and high dose groups were fed with high-fat diet. After 12 weeks

the Xiangsha Liu Junzitang low dose and high dose groups received corresponding dosage of drugs

while normal group

high fat group and spleen deficiency high fat group received corresponding volume of normal saline. After 4 weeks

the contents of total cholesterol (TC)

triglyceride (TG)

low density lipoprotein cholesterol cholesterol (LDL-C)

and high density lipoprotein cholesterol(HDL-C)were detected by automatic biochemistry analyzer

while D-xylose excretion rate was measured by phloroglucinol method. The morphological changes of liver cells were observed by hematoxylin eosin (HE) staining. The level of PON1

apoA1 and SAA in plasma were detected by enzyme-linked immunosorbent assay (ELISA). Paraoxonase 1(PON1)

apolipoprotein A1 (apoA1) and serum amyloid protein A (SAA) gene expression in rats liver were detected by Real-time fluorescence quantitative polymerase chain reaction (Real-time PCR).

Result:

2

As compared with normal group

the serum TC

TG

and LDL-C levels were significantly increased in the high-fat group and spleen-deficiency high-fat group (

P

<

0.05)

and HDL-C levels were significantly lower (

P

<

0.05); the levels of PON1 and apoA1 in plasma were decreased (

P

<

0.05)

while the content of SAA was increased (

P

<

0.05); the expression of SAA gene in liver tissues was increased (

P

<

0.01)

and the expression levels of PON1 and apoA1 genes in liver tissues were significantly decreased (

P

<

0.01). In high-fat group and the spleen-deficiency and high-fat group

the hepatocytes were rounded and scattered

and scattered fat vacuoles were observed. In addition

the urinary

D

-xylose excretion rate was significantly decreased in the spleen-deficiency and high-fat group (

P

<

0.05). After the intervention with Xiangsha Liu Junzitang

the serum TC

LDL-C levels were significantly decreased (

P

<

0.05); HDL-C levels were significantly increased (

P

<

0.05); plasma PON1

apoA1 levels were increased (

P

<

0.05); the content of SAA was decreased (

P

<

0.05); the expression of SAA gene in liver tissues was decreased (

P

<

0.05); the expression of apoA1 gene was increased significantly (

P

<

0.05). Liver cells swelling was significantly alleviated and fat foaming was reduced. As compared with high-fat group

the plasma PON1 and SAA levels in the spleen-deficiency high-fat group were significantly lower (

P

<

0.05); hepatocyte swelling was obvious and foaming was aggravated.

Conclusion:

2

The lipid disorder in hyperlipidemia rats was aggravated by the spleen deficiency

but was corrected after intervention with Xiangsha Liu Junzitang. and its mechanism may be related to the regulation of the expression of dyHDL-related genes and protein.