Objective To investigate the protective effect of folic acid(FA) on osteoporosis in ovariectomized(OVX) rats.Methods Forty three-month-old female SD Rats were divided into 5 groups, sham operation group, OVX group, diethylstilbestrol group(0.03mg·kg-1·d-1),low dose FA Group (5 mg·kg-1·d-1),and high dose FA group (20 mg·kg-1·d-1).Gastric gavage in each group was started from one week after being ovariectomized and lasted 10 weeks. Sham operation group and OVX group were treated with solvent. The rats were sacrificed at the end of 10th week after treatment. The total homocysteine(tHcy) in plasma, alkaline phosphatase(ALP), and tartrate-resistant acid phosphatase(TRACP) activity of bone homogenates were measured. The bone mineral density(BMD) and bone biomechanics were determined using L5 vertebrae and right femur. The bone tissue slices were made with L6 vertebrae and left femur and HE stained, and then the histomorphology was observed. Results Compared with sham operation group, plasma tHcy level was significantly increased(P＜0.01), BMD of lumbar vertebrae and femur was remarkedly decreased in OVX group(all P＜0.01). Plasma tHcy concentration was negatively correlated with lumbar BMD(r=-0.359, P=0.040). Plasma tHcy level in both groups treated with folic acid was significantly reduced(all P＜0.01). The ALP concentration in bone homogenates was higher, the TRACP concentration in bone homogenates was lower, and BMD and bone biomechanics of lumbar vertebrae and femur were increased in high dose FA group than those in OVX group(all P ＜0.01). Conclusions In OVX rats hyperhomocysteinemia existed and was involved in the development of osteoporosis. Folic acid could protect OVX rats from osteoporosis, due probably to improved homocysteine metabolism.

BACKGROUND: CpG oligonucleotide has been shown to strengthen the function of peripheral blood mononuclear cells (PBMCs), but its effects on type 1 diabetes mellitus has been rarely reported. OBJECTIVE: To investigate the effects of CpG oligonucleotide on the expression of interferon γ (IFN-γ), interleukin (IL) -12 and IL-10 in PBMCs in patients with type 1 diabetes mellitus versus healthy controls. METHODS: PBMCs were isolated from patients with type 1 diabetes mellitus and healthy controls and then cultured in RPMI-1640 with non-stimulator (control group) and CpG oligonucleotide (CpG oligonucleotide group), respectively. The mRNA expression of IFN-γ, IL-10, and IL-12 in PBMCs was detected by reverse transcription-polymerase chain reaction. RESULTS AND CONCLUSION: mRNA expression of IFN-γ and IL-10 was significantly lower in patients with type 1 diametes mellitus than in healthy controls (P < 0.01). In the CpG oligonucleotide group, the mRNA expression of IFN-γand IL-12 was significantly higher than in the healthy control group (P < 0.01), but the mRNA expression of IL-10 was similar to that in the healthy control group (P > 0.05). These findings demonstrated that CpG oligonucleotide can promote the production of IFN-γ and IL-12 in PBMCs of type 1 diametes mellitus.

Objective To study the effect of curcumin on the radiosensitivity of the human papillary thyroid cancer cell line TPC?1, to investigate the signaling pathway probably targeted by curcumin, and to provide new insights for the development of radiosensitizers for thyroid cancer. Methods The human papillary thyroid cancer cell line TPC?1 was treated with curcumin and radioactive iodine. CCK?8 assay, colony formation assay, and flow cytometry were used to evaluate cell proliferation, colony formation ability, and cell apoptosis, respectively. Western blot was used to measure the expression of p50, p65, and apoptosis?related proteins, Bcl?2 and Bax. Cell proliferation, colony formation ability, and cell apoptosis were determined again after the activity of the NF?κB signaling pathway was blocked by a NF?κB signaling pathway inhibitor PDTC. Results After treatment with curcumin and radioactive iodine, the human papillary thyroid cancer TPC?1 cells had reduced cell proliferation and colony formation, an elevated apoptosis rate, downregulated expression of anti?apoptotic Bcl?2, and upregulated expression of pro?apoptotic Bax in a dose?dependent manner. These results indicated that curcumin enhanced the radiosensitivity of TPC?1 cells. Curcumin inhibited the activation of the NF?κB signaling pathway in the TPC?1 cells treated with radioactive iodine. When the activity of the NF?κB pathway was blocked by PDTC, cell proliferation and colony formation were reduced and the apoptosis rate was increased, indicating an enhanced radiosensitivity of TPC?1 cells. Conclusions Curcumin is likely to target the NF?κB signaling pathway. It regulates the radiosensitivity of thyroid cancer cells by inhibiting the activity of the NF?κB signaling pathway.