Effects of transcutaneous electrical nerve stimulation on rats with the third lumbar vertebrae transverse process syndrome.

OBJECTIVE: To investigate the analgesic and anti-inflammatory effects of transcutaneous electrical nerve stimulation (TENS) at local or distant acupuncture points in a rat model of the third lumbar vertebrae transverse process syndrome. METHODS: Forty Sprague-Dawley rats were randomly divided into control, model, model plus local acupuncture point stimulation at BL23 (model+LAS) and model plus distant acupuncture point stimulation at ST36 (model+DAS) groups. All rats except controls underwent surgical third lumbar vertebrae transverse process syndrome modelling on day 2. Thereafter, rats in the model+LAS and model+DAS groups were treated daily with TENS for a total of six treatments (2/100 Hz, 30 min/day) from day 16 to day 29. Thermal pain thresholds were measured once a week during treatment and were continued until day 57, when local muscle tissue was sampled for RT-PCR and histopathological examination after haematoxylin and eosin staining. mRNA expression of interleukin-1 ß (IL-1ß), tumour necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS) was determined. RESULTS: Thermal pain thresholds of all model rats decreased relative to the control group. Both LAS and DAS significantly increased the thermal pain threshold at all but one point during the treatment period. Histopathological assessment revealed that the local muscle tissues around the third lumbar vertebrae transverse process recovered to some degree in both the model+LAS and model+DAS groups; however, LAS appeared to have a greater effect. mRNA expression of IL-1ß, TNF-α and iNOS in the local muscle tissues was increased after modelling and attenuated in both model+LAS and model+DAS groups. The beneficial effect was greater after LAS than after DAS. CONCLUSIONS: TENS at both local (BL23) and distant (ST36) acupuncture points had a pain-relieving effect in rats with the third lumbar vertebrae transverse process syndrome, and LAS appeared to have greater anti-inflammatory and analgesic effects than DAS. TRIAL REGISTRATION NUMBER: 09073.

Cigarette smoking and risk of hip fracture in women: a meta-analysis of prospective cohort studies.

BACKGROUND AND OBJECTIVES: Whether cigarette smoking can increase the risk of hip fracture in women is unclear. This meta-analysis, which pooled results from 10 prospective cohort studies, was performed to derive a more precise estimation between cigarette smoking and the risk of hip fracture in women. MATERIALS AND METHODS: Pubmed, Cochrane Central Register of Controlled Trials and ISI Web of Science were systematically searched to identify relevant studies. A meta-analysis was performed to examine the association among 10 studies. The pooled risk estimates were calculated by using both random- and fixed-effects model. Heterogeneity among articles and their publications bias were also tested. All of the statistical analyses were performed using the software programs STATA (version 12.0). RESULTS: Relative risk was significantly increased in current female smokers (pooled RR, 1.30; 95%CI, 1.16-1.45). The association was significant among the high-dose smokers (more than 15 cigarettes per day) while not among the low-does smokers (less than 15 cigarettes per day). Omission of any single study had little effect on the pooled risk estimate. Former smokers had a similar RR of hip fracture (RR, 1.02; 95%CI, 0.93-1.11) to published papers. Smoking cessation for ≥10 years leads to a significant decline in risk. CONCLUSIONS: Smoking is associated with an increased hip fracture risk in women. Cessation of smoking for ≥10 years had a decreased impact on risk of hip fracture. Given the inconsistency among the studies in the choice of adjustments, the associations between cigarette smoking and risk of hip fracture in women await further investigation.

Low-dose X-ray irradiation promotes osteoblast proliferation, differentiation and fracture healing.

Great controversy exists regarding the biologic responses of osteoblasts to X-ray irradiation, and the mechanisms are poorly understood. In this study, the biological effects of low-dose radiation on stimulating osteoblast proliferation, differentiation and fracture healing were identified using in vitro cell culture and in vivo animal studies. First, low-dose (0.5 Gy) X-ray irradiation induced the cell viability and proliferation of MC3T3-E1 cells. However, high-dose (5 Gy) X-ray irradiation inhibited the viability and proliferation of osteoblasts. In addition, dynamic variations in osteoblast differentiation markers, including type I collagen, alkaline phosphatase, Runx2, Osterix and osteocalcin, were observed after both low-dose and high-dose irradiation by Western blot analysis. Second, fracture healing was evaluated via histology and gene expression after single-dose X-ray irradiation, and low-dose X-ray irradiation accelerates fracture healing of closed femoral fractures in rats. In low-dose X-ray irradiated fractures, an increase in proliferating cell nuclear antigen (PCNA)-positive cells, cartilage formation and fracture calluses was observed. In addition, we observed more rapid completion of endochondral and intramembranous ossification, which was accompanied by altered expression of genes involved in bone remodeling and fracture callus mineralization. Although the expression level of several osteoblast differentiation genes was increased in the fracture calluses of high-dose irradiated rats, the callus formation and fracture union were delayed compared with the control and low-dose irradiated fractures. These results reveal beneficial effects of low-dose irradiation, including the stimulation of osteoblast proliferation, differentiation and fracture healing, and highlight its potential translational application in novel therapies against bone-related diseases.

The effects of low dose X-irradiation on osteoblastic MC3T3-E1 cells in vitro.

BACKGROUND: It has been indicated that moderate or high dose of X-irradiation could delay fracture union and cause osteoradionecrosis, in part, mediated by its effect on proliferation and differentiation of osteoblasts. However, whether low dose irradiation (LDI) has similar roles on osteoblasts is still unknown. In this study, we investigated whether and to what extent LDI could affect the proliferation, differentiation and mineralization of osteoblasts in vitro. METHODS: The MC3T3-E1 cells were exposed to single dose of X-irradiation with 0, 0.1, 0.5, 1.0 Gy respectively. Cell proliferation, apoptosis, alkaline phosphatase (ALP) activity, and mineralization was evaluated by methylthiazoletetrazolium (MTT) and bromodeoxyuridine (BrdU) assay, flow cytometry, ALP viability kit and von Kossa staining, respectively. Osteocalcin (OCN) and core-binding factor α1 (Cbfα1) expressions were measured by real time-PCR and western blot, respectively. RESULTS: The proliferation of the cells exposed to 2.0 Gy was significantly lower than those exposed to ≤1.0 Gy (p < 0.05) from Day 4 to Day 8, measured by MTT assay and BrdU incorporation. For cells exposed to ≤1.0 Gy, increasing dosages of X-irradiation had no significant effect on cell proliferation and apoptosis. Importantly, LDI of 0.5 and 1 Gy increased ALP activities and mineralized nodules of MC3T3-E1 cells. In addition, mRNA and protein expressions of OCN and Cbfα1 were also markedly increased after treatment with LDI at 0.5 and 1 Gy. CONCLUSIONS: LDI have different effects on proliferation and differentiation of osteoblasts from those of high dose of X-irradiation, which might suggest that LDI could lead to promotion of fracture healing through enhancing the differentiation and mineralization of osteoblasts.

Ginsenoside Rg1 promotes proliferation and neurotrophin expression of olfactory ensheathing cells.

Transplantation of olfactory ensheathing cells (OECs) is currently considered to be one of the most promising repair strategies for human spinal cord injury. However, the factors that regulate OECs are still poorly understood. Ginsenoside Rg1 (Rg1), the phytosterol from Panax ginseng, is a potent neuroprotective agent that promotes axonal regeneration. The aim of this study is to determine whether Rg1 would influence the biological activity of OECs. Primary cultured OECs from the olfactory bulb of neonatal rats were treated with Rg1 of various concentrations and durations. Using MTT and bromodeoxyuridine assays, we found that Rg1 significantly promoted cell proliferation, with an optimal concentration of 40 mug/ml of Rg1 at 72 h. In addition, RT-PCR and ELISA assays showed that Rg1 could upregulate the mRNA expression and secretion of glial cell-derived neurotrophic factor, brain-derived neurotrophic factor, and nerve growth factor. These results suggest that Rg1 may have a great potential in OEC therapy.