[Effect of atorvastatin on LOX-1 and eNOS expression in collateral vessels of hypercholesterolemic rats].

OBJECTIVE: To investigate the effect of atorvastatin on the expression of lectin- like oxLDL receptor 1 (LOX-1) and endothelial nitric oxide synthase (eNOS) in collateral vessels of hypercholesterolemic rats. METHODS: Forty male SD rats were randomized equally into 4 groups: femoral ligation group (L), hypercholesterolemia + femoral ligation group (HL), hypercholesterolemia+atorvastatin+femoral ligation group (AL), and hypercholesterolemia+normal saline+femoral ligation group (NL). The rats in the latter 3 groups were fed atherogenic diet for 8 weeks. At the end of the 8 weeks, the rats were subjected to femoral artery ligation with or without intraperitoneal injection of atorvastatin (AL group) or saline (NL group). Two weeks later, all the rats were euthanized and the expressions of LOX-1 and eNOS in the collateral vessels were detected with immunofluorescence assay. In the in vitro experiment, cultured human umbilical vein endothelial cells (HUVECs) were transfected with LOX-1 siRNA followed by treatment with oxLDL and/or atorvastatin. The expressions of LOX-1 and eNOS in the cells were detected with realtime PCR and Western blotting, and the cellular NO production was examined with Griess assay. RESULTS: The collateral vessels of rats with normal feeding expressed LOX-1, which was significantly increased in the collateral vessels of hypercholesterolemic rats; atorvastatin treatment significantly lowered LOX-1 expressions in the hypercholesterolemic rats. In normally fed rats, the growing collateral vessels exhibited strong eNOS expressions, which were lowered in hypercholesterolemic rats and enhanced after atorvastatin treatment. In the cell experiment, HUVECs with oxLDL treatment showed a high LOX-1 expression and a low eNOS expression, and atorvastatin treatment of the cells down-regulated LOX-1 and up-regulated eNOS expressions. Inhibition of LOX-1 mediated by a specific LOX-1 siRNA abolished the effect of oxLDL stimulation on eNOS expression in the cells. CONCLUSIONS: Both hypercholesterolemia and oxLDL can induce endothelial dysfunction and impair collateral vessel growth via the LOX-1/eNOS pathway in rats, and atorvastatin treatment can restore the LOX-1/eNOS pathway to promote the growth of the collateral vessels, suggesting the potential of atorvastatin as a therapeutic agent to promote repair of collateral vessel injuries in ischemic diseases.

Electroacupuncture and Waist-building Exercise in Treating Lumbar Disk Herniation / 针灸推拿医学（英文版）

Objective: To observe the clinical efficacy of electroacupuncture and waist-building exercise in treating lumbar disk herniation. Methods: A multi-center, randomized controlled trial was adopted. Three hundred cases of lumbar disk herniations were divided into two groups, an observation group in which 149 cases were treated by electroacupuncture and waist-building exercise, and a control group in which 151 cases were treated by electroacupuncture alone. The clinical efficacy and long-term relapse rate were observed and compared between the two groups. Results: Among 149 cases in the observation group, 80 cases were cured, 57 cases improved, 12 cases failed and 4 cases relapsed; the cure rate was 53.7%, the total effective rate was 91.9% and the relapse rate was 5.0%. Among 151 cases in the control group, 74 cases were cured, 51 cases improved, 26 cases failed and 12 cases relapsed; the cure rate was 49.0%, the total effective rate was 82.8% and the relapse rate was 16.2%. There were significant differences in the cure rate and the total effective rate between the two groups (P<0.05). Conclusion: Combined electroacupuncture and waist-building exercise had better effects than electroacupuncture in treating lumbar disk herniation.