[Biomechanical and biocompatible enhancement of reinforced calcium phosphate cement via RGD peptide grafted chitosan nanofibers].

Objective: To analysis the biomechanical and biocompatible properties of calcium phosphate cement (CPC) enhanced by chitosan short nanofibers(CSNF) and Arg-Gly-Asp (RGD). Methods: Chitosan nanofibers were prepared by electrospinning, and cut into short fibers by high speed dispersion. CPC with calcium phosphorus ratio of 1.5:1 was prepared by Biocement D method. The composition and structure of CPC, CSNF, RGD modified CSNF (CSNF-RGD), CSNF enhanced CPC (CPC-CSNF), RGD modified CPC-CSNF (CPC-CSNF-RGD) were observed by infrared spectrum, X-ray diffraction (XRD) and scan electron microscopy (SEM). The mechanical properties were measured by universal mechanical testing instrument. The adhesion and proliferation of MC3T3 cells were assessed using immunofluorescence staining and MTT method. Results: The distribution of CSNF in the scaffold was homogeneous, and the porous structure between the nanofibers was observed by SEM. The infrared spectrum showed the characteristic peaks at 1633 nm and 1585 nm, indicating that RGD was successfully grafted on chitosan nanofibers. The XRD pattern showed that the bone cement had a certain curability. The stain-stress test showed that break strengths were (17.74±0.54) MPa for CPC-CSNF and (16.67±0.56) MPa for CPCP-CSNF-RGD, both were higher than that of CPC(all P<0.05). The immunofluorescence staining and MTT results indicated that MC3T3 cells grew better on CPC-CSNF-RGD after 240 min of culture(all P<0.05). Conclusion: CSNF-RGD can improve the biomechanical property and biocompatibility of CPC, indicating its potential application in bone tissue repair.

Effect of B vitamin (folate, B6, and B12) supplementation on osteoporotic fracture and bone turnover markers: a meta-analysis.

BACKGROUND: B vitamins (including folate, B6, and B12) supplementation can effectively and easily modify high plasma homocysteine (Hcy). However, the role of Hcy in the pathogenesis of osteoporotic fracture and bone turnover is still controversial. This meta-analysis aimed to assess the impact of B vitamin supplementation on occurrence of any osteoporotic fracture and bone turnover by pooling the results of previous studies. MATERIAL AND METHODS: Relevant randomized controlled trials (RCTs) were searched in databases. Data integration and analysis were done by using Review Manager 5.3 (the Cochrane Collaboration). The risk ratio (RR) and corresponding 95% confidence intervals (CI) of fracture (intervention vs. control) were estimated. Changes in bone turnover indicators (continuous data), weighted mean difference (WMD), and corresponding 95% (CI) were pooled for estimation. RESULTS: Based on the results of 4 RCTs, this meta-analysis failed to identify a risk-reducing effect of daily supplementation of B vitamins on osteoporotic fracture in patients with vascular disease and with relatively normal plasma Hcy. In addition, we also did not find any positive effects of B vitamin supplementation on bone turnover. CONCLUSIONS: B vitamin supplementation might not be effective in preventing fracture and improving bone turnover. However, the possible benefits in selective populations, such as populations with very high plasma Hcy and from regions without B vitamin fortification should be explored in the future.

Comparison of Open Reduction and Internal Fixation with Plate and Titanium Elastic Intramedullary Nail in Treating Pediatric Humeral Fracture.

OBJECTIVE: To investigate the therapeutic efficacy of titanium elastic intramedullary nail (TEN) and open reduction and internal fixation with plate (ORIF) in the treatment of humeral fracture in children. METHODS: A retrospective study was carried out in a total of 69 patients who were admitted to the hospital from January 2013 to December 2018. These patients, including 41 males and 28 females, were aged from 6 to 12 years old with a median of 8 years. These patients were diagnosed with humeral fracture and underwent the surgery of ORIF (n = 22) or TEN (n = 47). The intraoperative bleeding, operation time, length of stay (LOS), and fracture healing time were compared between the two groups. The therapeutic effect was assessed by the shoulder range of motion, the elbow range of motion, the UCLA shoulder function score, and the Mayo elbow performance score (MEPS) 6 months after the surgery. RESULTS: The intraoperative bleeding (97.20 ± 27.83 mL vs 185.60 ± 37.50 mL, P < 0.05), the operation time (53.70 ± 11.87 min vs 73.50 ± 13.33 min, P < 0.05), and the fracture healing time (9.30 ± 4.23 weeks vs 13.45 ± 3.67 weeks, P < 0.05) in the TEN group was significantly decreased than those in the ORIF group. There was no significant difference in the LOS between the two groups. The length of follow-up is 3 and 6 months. The shoulder range of motion (110.88° ± 15.82° vs 98.37° ± 16.22° at 3 months and 162.88° ± 17.29° vs 117.65° ± 19.38° at 6 months, both P < 0.05), the elbow range of motion (105.23° ± 2.81° vs 87.12° ± 4.73° at 3 months and 137.47° ± 4.82° vs 109.67° ± 5.83° at 6 months, both P < 0.05), and the UCLA shoulder function score (28.58 ± 4.74 vs 21.64 ± 7.23 at 3 months and 33.05 ± 3.27 vs 25.78 ± 3.87 at 6 months, both P < 0.05), and the MEPS (80.76 ± 3.53 vs 65.33 ± 9.43 at 3 months and 97.48 ± 1.23 vs 88.22 ± 3.65 at 6 months, both P < 0.05) in the TEN group were greater than those in the ORIF group. In the TEN group, complications occurred in three of 47 cases (6.38%), including one case (2.13%) of bone nonunion and two cases (4.25%) of irritation response around the nail. In the ORIF group, complications occurred in four of 22 cases (18.18%), including one case (4.55%) of delayed healing, one case (4.55%) of deep infection, and two cases (9.08%) of radial nerve injury. The complication rate was not significantly different between the two groups. CONCLUSION: TEN can be a good technique for the treatment of humeral fracture in children, with the advantages of less intraoperative bleeding, shorter operative time, quicker healing, and better recovery of shoulder range of motion and elbow range of motion.

lncRNA myocardial infarction-associated transcript (MIAT) knockdown alleviates LPS-induced chondrocytes inflammatory injury via regulating miR-488-3p/sex determining region Y-related HMG-box 11 (SOX11) axis.

Long noncoding RNA (lncRNA) has been shown to be involved in the development of osteoarthritis (OA), an age-related bone and joint disease. However, the function and possible molecular mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in lipopolysaccharide (LPS)-induced chondrocytes injury model remain unexplored. Cell viability and apoptosis were detected by methyl thiazolyl tetrazolium (MTT) and flow cytometry, respectively. Western blot was used to detect protein expression. The concentrations of inflammatory factors were estimated by enzyme-linked immunosorbent assay (ELISA). Abundances of MIAT, microRNA-488-3p (miR-488-3p), and sex determining region Y-related HMG-box 11 (SOX11) were examined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to analyze the interaction between miR-488-3p and MIAT or SOX11. LPS caused chondrocytes injury by reducing cell activity and increasing apoptosis rate and inflammatory factor secretions. Higher levels of MIAT and SOX11 and lower miR-488-3p were observed in LPS-treated C28/I2 cells. Importantly, knockdown of MIAT attenuated the LPS-induced cell injury by targeting miR-488-3p, and miR-488-3p overexpression weakened the LPS-induced cell injury by targeting SOX11. Additionally, repression of MIAT inactivated the LPS-induced NF-κB signaling pathway by decreasing SOX11 and increasing miR-488-3p. Knockdown of MIAT alleviated the LPS-induced chondrocytes injury by inhibiting the NF-κB signaling pathway mediated by the miR-488-3p/SOX11 axis.

Punicalagin Inhibits Tert-Butyl Hydroperoxide-Induced Apoptosis and Extracellular Matrix Degradation in Chondrocytes by Activating Autophagy and Ameliorates Murine Osteoarthritis.

BACKGROUND: Osteoarthritis (OA) is a prevalent articular disorder and has no entirely satisfactory treatment. Punicalagin (PUG) is a polyphenol which has shown multiple pharmacological effects on various diseases. However, the role of PUG in the treatment of OA has not been well defined. METHODS: The effects of PUG on anti-oxidative stress, anti-apoptosis, extracellular matrix (ECM) degradation and autophagy were evaluated in chondrocytes through Western blot and immunofluorescence (IF) staining. Meanwhile, the effects of PUG on destabilization of the medial meniscus (DMM) model were also assessed in vivo by performing histopathologic analysis and IF staining. RESULTS: In vitro, PUG treatment not only increased the level of HO-1 and SOD1 against oxidative stress but also suppressed the expression of apoptotic proteins and inhibited ECM degradation. Meanwhile, PUG treatment activated autophagy and restores autophagic flux in chondrocytes after tert-butyl hydroperoxide (TBHP) insult, inhibition of autophagy by 3-methyladenine (3-MA) partly abrogated the protective effects of PUG on chondrocytes. In vivo, degeneration of the articular cartilage following DMM was also ameliorated by PUG treatment. CONCLUSION: PUG prevents the progression of OA through inhibition of apoptosis, oxidative stress and ECM degradation in chondrocytes, which mediated by the activation of autophagy.

Triptolide Suppressed the Microglia Activation to Improve Spinal Cord Injury Through miR-96/IKKß/NF-κB Pathway.

STUDY DESIGN: The effect of triptolide on spinal cord injury (SCI) and inflammatory response was observed by establishing SCI rat model. And in vitro experiments were conducted to determine the underlying mechanism of triptolide-mediated in murine microglial cell line BV2. OBJECTIVE: To determine the underlying mechanism of triptolide in suppressing the microglia activation to improve SCI. SUMMARY OF BACKGROUND DATA: Triptolide, as a major active ingredient of Chinese herb Tripterygium wilfordii, can promote spinal cord repair through inhibiting microglia activation, but the underlying mechanism is not clear. METHODS: Locomotion recovery was accessed by Basso, Beattie, and Bresnahan score, the number of footfalls, stride length, and angle of rotation analysis. Expressions of microRNA 96 (miR-96), microglia activation marker Iba-1, and IκB kinase (IKKß)/nuclear factor (NF)-κB-related proteins were detected by qRT-PCR or western blot. Inflammatory cytokines tumor necrosis factor-α and interleukin -1ß were measured by enzyme-linked immuno sorbent assay. The regulation of miR-96 on IKKß was confirmed by dual luciferase reporter assay. RESULTS: Triptolide promoted locomotion recovery of SCI rats, upregulated the expression of miR-96, decreased microglia activation marker Iba-1 and IKKß/NF-κB-related proteins, and inhibited inflammatory cytokines tumor necrosis factor-α and interleukin-1ß levels in spinal cord tissues and lipopolysaccharide -induced microglia. Triptolide suppressed the microglia activation and inflammatory cytokines secretion in BV2 cells through up-regulating miR-96. We confirmed the interaction between miR-96 and IKKß, and IKKß expression was negatively regulated by miR-96. Finally, we determined that triptolide suppressed the microglia activation and inflammatory cytokines secretion through miR-96/IKKß pathway. CONCLUSION: Triptolide suppressed microglia activation after SCI through miR-96/IKKß/NF-κB pathway. LEVEL OF EVIDENCE: N/A.