Effect of increased levels of adiponectin by administration of the adenovector rAAV2/1-Acrp30 on glucose, lipid metabolism and ultrastructure of the aorta in Goto–Kakizaki rats with arteriosclerosis.

Background. We used recombinant adeno-associated virus vector of adiponectin (AAV2/1-Acrp30) to study the effects of increased levels of adioponectin (by the administration of rAAV2/1-Acrp30) on arteriosclerosis, glucose and lipid metabolism in Goto–Kakizaki (GK) rats with arteriosclerosis. Methods. Thirty GK rats with arteriosclerosis were divided into 3 equal groups: control group 1, control group 2 and the rAAV2/1-Acrp30-administered group. Saline, virus vector or rAAV2/1-Acrp30 (1012 ng/ml) vector genomes administered to the rats in the corresponding group by intramuscular injection to the posterior limb by single administration, respectively. After 8 weeks, fasting blood glucose, 2-hour postprandial blood glucose, glycosylated haemoglobin, serum insulin, serum total cholesterol, triglycerides, high-density lipoprotein and low-density lipoprotein were measured in each group, and the ultrastructure of the aorta was seen by light and electron microscopy. Results. Compared with control groups 1 and 2, in the rAAV2/1-Acrp30 group, there was a decrease in urine volume, fasting blood glucose, 2-hour postprandial blood glucose, glycosylated haemoglobin, serum total cholesterol, triglycerides and low-density lipoprotein, and an increase in body weight and high-density lipoprotein (p<0.05), while the level of serum insulin was not changed (p>0.05). Ultrastructure studies of the aorta showed that aortosclerosis in the rAAV2/1-Acrp30-administered group was less, and fewer lipid droplet vacuoles were seen in the vascular endothelial cytoplasm. Also various cell organelles and internal elastic lamina were seen, and there was no formation of lipid droplet and foam cells in the cytoplasm of the media of the smooth muscle. Conclusion. Adiponectin could improve blood glucose and lipid parameters and decrease atherosclerosis in the aorta of GK rats.

Experimental research on immunological activity of Polyactin A.

Polyactin A is a polysaccharide extracted from cultured alpha-Streptococcus No. 33 in the mouth. It is also known as alpha-glucomannan. According to clinical reports, Polyactin A is considered to be an immunological adjuvant with significant curative effect in chemotherapy of tumors. Immunological activities of Polyactin A were studied. When injected into mice at the dosage of 100 mg/kg for 4-5 consecutive days, Polyactin A can cause a marked increase in spleen weight and RFC in spleen, and it can antagonize the immunosuppressive actions of cyclophosphamide. Polyactin A can also increase phagocytosis of macrophages in the peritoneal cavity of mice. Phagocytotic ratio and phagocytotic index in the experimental group were greater than those in the control group. Phagocytotic ratio and phagocytotic index were respectively 63.5 +/- 8.3% and 1.02 +/- 0.05% in the Polyactin A treated group but were respectively 21.0 +/- 5.7% and 0.3 +/- 0.03% in the control group. The differences were significant (p < 0.05, < 0.01). Polyactin A had definite influence on the transformation test of lymphocytes and increased the transformation ratio of lymphocytes in vitro. The ability of Polyactin A to induce the transformation of lymphocytes into lymphoblasts was almost the same as that of PHA. These results suggest that polyactin A has a marked immunological activity, which is not entirely due to the role of large molecular weight polysaccharide. They provide direct evidence for the assumption that Polyactin A may be an immunological adjuvant, and it is experimentally confirmed that Polyactin A can protect the immunity of the organism.