Effect of Jianpi Huogu Formula on function damage of vascular endothelial cells induced by glucocorticoid / 中国中药杂志

This study aimed to observe the intervention effect of Jianpi Huogu Formula(JPHGF) on the functional damage of vascular endothelial cells caused by glucocorticoid, and explore its action mechanism from the PI3 K/Akt and mitogen activated protein kinase(MAPK) signaling pathways. The extracted thoracic aorta ring of normal SD rats were intervened first with vascularendothelial growth factor(VEGF, 20 μg·L-1) and/or sodium succinate(MPS, 0. 04 g·L-1) in vitro and then with JPHGF(8, 16, and 32 μg·L-1) for five mcontinuous ethylpdays, rednisolofollowed nebythe statistics of the number, length, and area of microvessels budding fromvascular rings. In addition, the human umbilical vein endothelial cells(HUVECs) induced by VEGF(20 μg·L-1) were added with MPS(0. 04 g·L-1) and then with JPHGF(8, 16, and 32 μg·L-1) for observing the migration, invasion, and luminal formation abilities of HUVECs in the migration, invasion and luminal formation experiments. The protein expression levels of PI3 K, p-Akt, p-JN K, and p-ERK in HUVECs were assayed by Western blot. The results showed that JPHGF dose-dependently improved the num-ber,length, and area of microvessels in MPS-induced rat thoracic aortic ring, reversed the migration, invasion and lumen formation abiliti es of HUVECs reduced by MPS, and up-regulated the protein expression levels of PI3 K, p-Akt, and p-JNK in HUVECs. All thesehave suggested that JPHGF exerts the protective effect against hormone-induced damage to the angiogenesis of vascular endothelial cells by activating the PI3 K/Akt and MAPK signaling pathways, which has provided reference for exploring the mechanism of JPHGF in treating s teroid-induced avascular necrosis of femoral head(SANFH) and also the experimental evidence for enriching the scientific connotationof spleen-invigorating and blood-activating therapy.

Effect of platelet rich plasma combined with core decompression on the repair of steroid-induced avascular necrosis of the femoral head and the MMP/TIMP in rabbits / 中国比较医学杂志

Objective To observe the effect of platelet rich plasma(PRP)combined with core decompression on the steroid-induced avascular necrosis of the femoral head(SANFH)and on MMP/TIM in rabbits.Methods A total of 42 New Zealand white rabbits were used in this study,and were randomly divided into 3 groups(decompression,combination and control groups,each n=14). The rabbit model of SANFH was established by i.m. injecting prednisolone acetate in the decompression group and combination group. The improved Landesberg method was used to make the platelet rich plasma. The decompression group received core decompression treatment while the combination group received PRP combined with core decompression for bone repair. X-ray photography of the hip joint of the two groups were taken at 2,6 and 10 weeks after the surgery,and the Lane-Sandhu X-ray scores and new bone area ratio were compared. Venous blood samples of the 3 groups were collected and the bilateral femoral heads were taken for further examination. The left femoral heads were used for histopathological observation and the right ones were used to determine the expression of the mRNA of MMP-2,MMP-9, TIMP-1, and TIMP-2. Results The levels of MMP-2 and MMP-9 in the decompression group were higher than that in the combination group and control group after surgery. The levels of TIMP-1 and TIMP-2 in the decompression group were significantly lower than the combination group and control group(P < 0.05). The IL-6 level and the rate of empty bone lacunae in the decompression group were significantly higher than the combination group and control group(P < 0.05), and that of the combination group was higher than the control group(P < 0.05). The combination group had a better joint imaging and histopathological evaluation than the decompression group after surgery. Conclusions Our findings demonstrate that PRP combined with core decompression can exert a positive effect on the MMP/TIMP and bone tissue repair in the treatment of steroid-induced avascular necrosis of the femoral head in rabbits.