Objective To investigate the influence of Ginkgo biloba L. extract (EGB) on the expression of apoptosis-related protein and NF-κB signaling pathway in the spleen tissue of mice with radiation damage. Methods The mice were divided randomly into normal control group (NC), irradiation control group (IC), low dose EGB group (IC+EGBL), medium dose EGB group (IC+EGBM) and high dose EGB group (IC+EGBH) according to the random number table, with 12 rats in each group. The mice in the low, middle and high dose EGB groups were given EGB respectively by 5, 10, 20 mg/kg, and the normal and irradiation control group were given saline by intraperitoneal injection once daily for 14 days. On the 15th day, the mice in all groups were uniformly irradiated with 4.0 Gy γ-rays for one time except normal control group. After 24 hours, Bcl-2, Bax and caspase-3 protein expression were measured by immunohistochemical method. The IKKβ expression was detected by qRT-PCR method, and the content of NF-κB p65 and IKKα in serum was detected by Elisa method in spleen tissue. Results Comparing with IC group, the expression of Bax (54.31 ± 1.59, 42.04 ± 1.56, 32.08 ± 2.43 vs. 68.68 ± 3.12) and caspase-3 protein (55.73 ± 2.61, 45.81 ± 2.59, 36.78 ± 2.23 vs. 72.18 ± 1.84) in IC+EGBL, IC+EGBM and IC+EGBH group were significantly decreased (P<0.05), the expression of Bcl-2 protein (30.33 ± 1.28, 39.80 ± 2.86, 44.42 ± 3.64 vs. 22.80 ± 2.01) in IC+EGBL, IC+EGBM and IC+EGBH group significantly increased (P<0.05), the expression of IKKβ mRNA (1.43 ± 0.06, 1.31 ± 0.06, 1.17 ± 0.09 vs. 1.64 ± 0.10) and the level of NF-κB p65 (129.38 ± 8.41 pg/ml, 111.28 ± 9.09 pg/ml, 95.41 ± 6.88 pg/ml vs. 145.64 ± 6.29 pg/ml) and IKKα (160.10 ± 8.94 pg/ml, 144.00 ± 8.36 pg/ml, 108.84 ± 13.74 pg/ml vs. 176.38 ± 8.54 pg/ml) in IC+EGBL, IC+EGBM and IC+EGBH group significantly decreased (P<0.05). Conclusions The EGB can reduce the expression of apoptotic protein Bax and caspase-3 in spleen cells induced by radiation, elevate the expression level of apoptotic protein Bcl-2, and inhibit the damage caused by radiation by regulating NF-κB signaling pathway.

BACKGROUND: In the process of bone defect healing, the use of biological materials loaded with drugs for local defect intervention can accelerate the repair of the defect, which provides a new method for the local treatment of bone defects. OBJECTIVE: To introduce the local application of bone tissue engineering scaffolds loaded with bisphosphonates in bone defect repair and to summarize the effects of bone tissue engineering scaffolds as a drug delivery system on the bone defect healing. METHODS: The authors retrieved PubMed, Web of Science, Springerlink, Medline, WanFang and CNKI databases with "bisphosphonates, alendronate, zoledronate, bone defect, bone tissue engineering" as key words for relevant articles published from 2006 to 2018. Initially, 235 articles were retrieved, and finally 70 articles were selected for further analysis. RESULTS AND CONCLUSION: Bisphosphonate drug is an effective inhibitor of osteoclast dissolution. It can form a drug sustained release system on the local defect by being loaded to composite scaffolds, promote the formation of new bone and accelerate the healing of the defect. For the drug delivery system of bisphosphonates, suitable scaffold materials are crucial to the osteogenic effect of composite scaffolds in the defect area. At present, the carrier materials used for bisphosphonate-loaded composite scaffolds are mainly divided into organic materials and inorganic materials. Most polymeric organic materials can directly load bisphosphonates to form good drug sustained release in the local area and obviously exert their pro-osteogenic effects, while natural materials and most inorganic materials are often combined with other materials to form composite materials as carriers to optimize the carrier performance. Most studies have also confirmed that these composite materials loaded with bisphosphonates in the defect area exert osteogenic effect in the defect area.