Homeopathic Ankle Dislocation for Treatment of Unstable Trimalleolar Fractures Involving Posterior Die-Punch Fragment: A Retrospective Cohort Study.

OBJECTIVES: Unstable trimalleolar fractures are relatively complex and more difficult to manage if die-punch fracture is present. We aimed to evaluate the curative effect of homeopathic ankle dislocation on the unstable trimalleolar fractures involving posterior die-punch fragments. METHODS: A total of 124 patients diagnosed with unstable trimalleolar fractures combined with post-die punch fragment between June 2008 and June 2020 were retrospectively included. Patients who received homeopathic ankle dislocation were named as the experimental group, and patients who accepted conventional treatment were control group. The fracture healing time, wound healing, American Orthopedic Foot and Ankle Society ankle-hindfoot scale (AOFAS), visual analogue scale (VAS), the Kellgren-Lawrence arthritis grading scale (KLAGS) and short-form 36 score (SF-36) scores were collected. Student t-test was used for fracture healing time. Wound healing and SF-36 were compared using the Mann-Whitney test. Repeated measurement analysis of variance (ANOVA) was used for AOFAS and VAS. χ2-test was used for KLAGS. RESULTS: AOFAS showed statistically significant differences between the two groups (p = 0.001). In non-weight-bearing and weight-bearing conditions, VAS scores were significant different between the two groups, and there was an interaction between group and time point (p < 0.001). The experimental group was superior to the control group in terms of physical function (p = 0.022), role-physical (p = 0.018), general health (p = 0.001) and social function (p = 0.042).The operation time of experimental group was shorter than that of control group (p < 0.001). CONCLUSION: Homeopathic ankle dislocation is used for the unstable trimalleolar fractures involving posterior die-punch fragment, which can provide better functional outcomes while shortening the operation time and recovery period.

Puerarin inhibits iNOS, COX-2 and CRP expression via suppression of NF-κB activation in LPS-induced RAW264.7 macrophage cells.

Puerarin (7,4'-dihydroxy-8-C-glucosylisoflavone) is the most abundant isoflavone-C-glucoside extracted from Radix puerariae, and it has been used for various medicinal purposes in traditional oriental medicine for thousands of years. In the present study, the ability of the puerarin to modulate inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and C reactive protein (CRP) expression and induce changes in the nuclear factor κB (NF-κB) pathway in RAW264.7 macrophage cells was examined. The protein and mRNA levels of lipopolysaccharide (LPS)-induced iNOS, COX-2 and CRP were determined in RAW246.7 macrophage cells. Inhibitor κB (I-κB) phosphorylation and p65NF-κB expression in RAW246.7 macrophage cells were also detected under our experimental conditions. The results indicated that puerarin inhibited the expression of LPS-induced iNOS, COX-2 and CRP proteins and also suppressed their mRNAs from RT-PCR experiments in RAW264.7 cells. Subsequently, we determined that the inhibition of iNOS, COX-2 and CRP expression was due to a dose-dependent inhibition of phosphorylation and degradation of I-κB, which resulted in the reduction of p65NF-κB nuclear translocation. These data suggested that the effect of puerarin-mediated inhibition of LPS-induced iNOS, COX-2 and CRP expression is attributed to suppressed NF-κB activation at the transcriptional level.

Puerarin inhibits C-reactive protein expression via suppression of nuclear factor kappaB activation in lipopolysaccharide-induced peripheral blood mononuclear cells of patients with stable angina pectoris.

Puerarin (4'-7-dihydroxy-8-beta-D-glucosylisoflavone), the most abundant isoflavone-C-glucoside extracted from the root of the plant Pueraria lobata, has demonstrated anti-inflammatory activity in cellular models of inflammation. In this report, we examined the ability of puerarin to modulate C-reactive protein (CRP) expression and key molecules in the nuclear factor kappa B (NF-kappaB) pathway to determine its molecular target. The protein and mRNA levels of CRP were determined in lipopolysaccharide (LPS)-induced peripheral blood mononuclear cells of patients with unstable angina pectoris. Also, we detected the I-kappaBalpha phosphorylation and the p65NF-kappaB expression in peripheral blood mononuclear cells under our experimental condition. The results indicated that puerarin inhibited the expression of the protein and mRNA levels of CRP in LPS-induced peripheral blood mononuclear cells. Subsequently, we determined that the inhibition of CRP expression was because of a dose-dependent inhibition of phosphorylation and degradation of inhibitor kappaB(I-kappaB), which resulted in a reduction of p65NF-kappaB nuclear translocation. We conclude that puerarin acts as an anti-inflammatory agent by blocking NF-kappaB signalling, and may possibly be developed as a useful agent for the chemoprevention of atherosclerosis.