Different concentrations of 17ß-estradiol modulates apoptosis induced by interleukin-1ß in rat annulus fibrosus cells.

Interleukin­1ß (IL­1ß) is a pleiotropic cytokine that mediates inflammatory and cell death activities. IL­1ß has been previously reported to induce apoptosis of intervertebral disc (IVD) cells in IVD degeneration. Accumulating data have suggested that post­menopausal women have a high incidence of IVD degeneration. It has therefore been proposed that estrogen may have a close association with IVD degeneration. Whether estrogen is able to protect IVD cells from apoptosis remains unclear. The present study aimed to examine whether 17ß­estradiol (17ß­E2) inhibited IL­1ß­induced apoptosis of rat annulus fibrosus (AF) cells. Additionally, the dose­response effect of 17ß­E2 on cell apoptosis was investigated. AF cells were isolated from male Sprague Dawley rats and cultured in complete medium. Following approximately two weeks, the AF cells were treated with IL­1ß (75 ng/ml) for 24 h, with a pretreatment of 17ß­E2 for 1 h. Apoptosis of AF cells was analyzed by annexin V/propidium iodide binding assay and morphological changes, together with an assessment of caspase­3 activity. Cell viability of the AF cells was determined by MTT assay. The level of apoptosis and caspase­3 activity in the AF cells was increased whereas the cell viability was decreased following treatment with IL­1ß (75 ng/ml), as compared with the control group. This effect was reversed by pretreatment with 17ß­E2, in a dose­dependent manner. The protective effect of 17ß­E2 was abolished by estrogen receptor antagonist ICI182, 780. These results indicate that 17ß­E2 protects rat AF cells from apoptosis induced by IL­1ß, in a dose­dependent manner.

17ß-Estradiol protects against apoptosis induced by levofloxacin in rat nucleus pulposus cells by upregulating integrin α2ß1.

Levofloxacin has been reported to have cytotoxicity to chondrocytes in vitro. And 17ß-estradiol has been widely studied for its protective effects against cell apoptosis. Based on apoptotic cell model induced by levofloxacin, the purpose of this study was to explore the mechanism by which 17ß-estradiol protects rat nucleus pulposus cells from apoptosis. Inverted phase-contrast microscopy, flow cytometry, and caspase-3 activity assay were used to find that levofloxacin induced marked apoptosis, which was abolished by 17ß-estradiol. Interestingly, estrogen receptor antagonist, ICI182780, and functional blocking antibody to α2ß1 integrin, both prohibited the effect of 17ß-estradiol. Simultaneously, levofloxacin decreased cellular binding ability to type II collagen, which was also reversed by 17ß-estradiol. Furthermore, western blot and real-time quantitative PCR were used to find that integrin α2ß1 was responsible for estrogen-dependent anti-apoptosis, which was time-response and dose-response effect. 17ß-estradiol was proved for the first time to protect rat nucleus pulposus cells against levofloxacin-induced apoptosis by upregulating integrin α2ß1 signal pathway.

Epidemiology and risk factors of cervical spine injury during heating season in the patients with cervical trauma: a cross-sectional study.

PURPOSE: The purpose of this study was to describe the epidemiology of cervical spine injury in the patients with cervical trauma and analyze its associated risk factors during the special heating season in North China. METHODS: This cross-sectional study investigated predictors for cervical spine injury in cervical trauma patients using retrospectively collected data of Hebei Provincial Orthopaedic Hospital from 11/2011 to 02/2012, and 11/2012 to 02/2013. Binary logistic regression analysis was used to determine risk factors for cervical fractures/dislocations or cord injury. RESULTS: A total of 106 patients were admitted into this study. Of all, 34 patients (32.1%) were treated from 11/2011 to 02/2012 and 72 patients (67.9%) from 11/2012 to 02/2013. The mean age was 41.9±13.3 years old; 85 patients (80.2%) were male and 82 (77.4%) from rural areas. Eighty patients (75.5%) were caused by fall including 45 (42.5%) by severe fall (>2 m). Sixty-five patients (61.3%) of all suffered injuries to other body regions and 32 (30.2%) got head injury. Thirty-one patients (29.2%) sustained cervical cord injury with cervical fractures/dislocations. Twenty-six (83.9%) of cervical cord injury patients were from rural areas and 24 (77.4%) of those resulted from fall including 15 (48.4%) from severe fall (>2 m). Logistic regression displayed that age (OR, 1.47; 95% CI, 1.05-2.07), head injury (OR, 5.63; 95% CI, 2.23-14.26), were risk factors for cervical cord injury and snowing (OR, 8.25; 95% CI, 2.26-30.15) was a risk factor for cervical spine injury due to severe fall (>2 m). CONCLUSIONS: The elder male patients and patients with head trauma are high-risk population for cervical cord injury. As a seasonal factor, snowing during heating season is of note a risk factor for cervical spine injury resulting from severe fall (>2 m) in the patients with cervical trauma in North China.