Protective effect of tongxinluo superfines on angiotensin II caused renal injury in rat / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore the renal protective effect of Tongxinluo (TXL) and its mechanism of action.</p><p><b>METHODS</b>Eight-week old SD rats were divided into the sham-operated group (A), the model group (B) and the TXL group, 6 rats in each group. Angiotensin II (Ang II) was administered slowly (200 ng/kg per min) to rats in group B and C via subcutaneously embedded osmotic pump to make them stimulative model of renal injury, while to rats in group A, pump embedding with saline infusion. After modeling, TXL was given to group C by gastric perfusion in dosage of 0.8 g/kg per day. And the following indexes were observed 14 days later: configuration of renal arterial endothelium by transmission electron microscope; pathologic figure of kidney with HE stain; renal apoptosis by TUNEL; expression of p53 and p22phox by RT-PCR;and level of reactive oxygen species (ROS) in kidney.</p><p><b>RESULTS</b>Different degree of congestion, swelling, denudation of endothelial cell in renal arterial endothelial cell; glomerular matrix proliferation and partial glomerular atrophy with tendency of fibrosis; increased renal parenchymal apoptosis; enhanced expression of p53 and p22phox; and elevated ROS were found in model animals. All the above-mentioned abnormalities, including glomerular injury, renal cell apoptosis, as well as the increased p53, p22phox expressions and ROS production were all alleviated in group C after TXL treatment.</p><p><b>CONCLUSION</b>TXL could protect renal against Ang II injury, and it may be realized by inhibiting NADPH-ROS/p53 pathways and suppressing cell apoptosis in renal parenchyma.</p>

Involvement of p53-dependent pathway in the antiproliferative activity of emodin in human smooth muscle cell / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate whether p53 pathway participates in the effect of emodin on vascular smooth muscle cell proliferation.</p><p><b>METHODS</b>The effects of emodin on vascular smooth muscle cell proliferation were evaluated by cell count, senescent-associated beta-galactosidase staining, and annexin V staining. DNA synthesis was determined by (3)H-thymidine corporation, cell cycle was analyzed by FACS, the p53 protein level was measured by Western blot and cDNA expression array technology was used to demonstrate the effect of emodin on the simultaneous expression of a large number of genes in cultured vascular smooth muscle cells.</p><p><b>RESULTS</b>Emodin at 1.6-3.1 microg/ml inhibited VSMC growth, at 6.3-12.5 microg/ml promoted VSMC aging and induced VSMC apoptosis at 25.0 microg/ml 24 hours after exposure. Unscheduled DNA synthesis, which was a sensitive indicator for DNA injury, was observed in VSMC following 24 hours emodin exposure. The mRNA and protein levels of p53 were up-regulated in a concentration-dependent manner. Proliferation/carcinogenesis-related genes were down-regulated and other genes related to cell senescence, apoptosis, and DNA damage/repair were up-regulated in VSMC after exposure to emodin for 24 hours. Emodin readily permeated VSMC membrane and mostly located in the cytoplasm and few of them in the nucleus.</p><p><b>CONCLUSIONS</b>The p53 pathway in VSMC was activated post emodin exposure in a concentration-dependent manner and which might be responsible for the observed antiproliferative effects of emodin in vascular smooth muscle cells.</p>