BABY BOOM (BBM), initially identified in Brassica napus, can enhance the shoot regeneration capacity in tissue culture and is involved in the conversion from the vegetative to embryogenic state. This study aimed to isolate BBM orthologue genes from Rosa canina and analyse their functions. Two full-length cDNAs, designated RcBBM1 and RcBBM2, were isolated from R. canina by the rapid amplification of cDNA ends (RACE). The predicted amino acid sequences of the two RcBBMs contained the bbm-1 motif and the motifs typically conserved in the eudicotANT (euANT) lineage. Phylogenetic tree analysis showed that the RcBBMs were most closely related to the BBM orthologue genes identified in Glycine max and Medicago truncatula. The transcripts of the RcBBMs were detected in young roots, calluses, and protocorm-like bodies (PLBs), whereas they were undetectable in stems, leaves, and flowers. RcBBM1-GFP and RcBBM2-GFP fusion proteins were both localized in the nucleus. 35S::RcBBM1 and 35S::RcBBM2 transgenic Arabidopsis thaliana lines exhibited enhanced shoot regeneration capacity in tissue culture, but did not undergo spontaneous somatic embryogenesis. The results suggest that RcBBMs may be candidate genes for improving the shoot regeneration efficiency of R. canina.

Intervertebral disc degeneration (IDD) is the main cause of low back pain. An increasing number of studies have suggested that inflammatory response or the senescence of nucleus pulposus (NP) cells is strongly associated with the progress of IDD. Eupatilin, the main flavonoid extracted from Artemisia, was reported to be associated with the inhibition of the intracellular inflammatory response and the senescence of cells. However, the relationship between eupatilin and IDD is still unknown. In this study, we explored the role of eupatilin in tumor necrosis factor-α (TNF-α)-induced activation of inflammatory signaling pathways and NP cell senescence, in the anabolism and catabolism of NP cell extracellular matrix (ECM) and in the effect of the puncture-induced model of caudal IDD in the rat. In vitro, eupatilin significantly inhibited TNF-α-induced ECM degradation, downregulated the expression of related markers of NP cells (MMP3, MMP9, and MMP13), and upregulated the expression of SOX9 and COL2A1. Furthermore, eupatilin reduced TNF-α-induced cell senescence by inhibiting the expression of the senescence of NP cell-related markers (p21 and p53). Mechanistically, ECM degradation and cell senescence were reduced by eupatilin, which inhibited the activation of MAPK/NF-κB signaling pathways. Consistent with the in vitro data, eupatilin administration ameliorated the puncture-induced model of caudal IDD in the rat. In conclusion, eupatilin can inhibit the inflammatory response and the senescence of NP cells, which may be a novel treatment strategy for IDD.

The aim of the current study was to investigate luteolin-induced apoptosis and the molecular mechanisms underlying it in HT29 cells. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to assess the cytotoxicity of luteolin on HT29 cells, and a dichloro-dihydro-fluorescein diacetate assay was used to measure cellular levels of reactive oxygen species (ROS). The effects of luteolin on the mitochondrial membrane potential were also evaluated. Bax and Bcl-2 mRNA expression were determined using reverse transcription-quantitative PCR. Additionally, western blot analysis was performed to assess changes in cytochrome c and caspase-3 protein expression. Localization of nuclear factor erythroid 2-related factor 2 (Nrf2) in the nucleus was also assessed using immunofluorescence. Luteolin exhibited cytotoxicity on HT29 cells in a time-and concentration-dependent manner. Additionally, ROS production was indicated to be increased and ROS scavenging was decreased, which resulted in a significant increase in the levels of ROS in the cells. The mitochondrial membrane potential was indicated to decrease following luteolin treatment. At the molecular level, luteolin significantly increased the mRNA expression of Bax and the protein expression of cytochrome c, caspase-3, p47 phox and p22 phox . The results revealed that luteolin decreased Bcl-2 protein expression and inhibited the nuclear localization of Nrf2. In conclusion, the current study indicated that luteolin inhibited HT29 cell proliferation and induced apoptosis via the mitochondrial pathway.

Background. Many studies have demonstrated that vitamin D has clinical benefits when used to treat patients with chronic obstructive pulmonary disease (COPD). However, most of these studies have insufficient samples or inconsistent results. The aim of this meta-analysis was to evaluate the effects of vitamin D therapy in patients with COPD. Methods. We performed a comprehensive retrieval in the following electronic databases: PubMed, Embase, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang Data, and Chinese Scientific Journals Database (VIP). Two trained reviewers identified relevant studies, extracted data information, and then assessed the methodical quality by the Cochrane risk of bias assessment tool, independently. Then, the meta-analyses were conducted by RevMan 5.4, binary variables were represented by risks ratio (RR), and continuous variables were represented by mean difference (MD) or standardized mean difference (SMD) to assess the efficacy of vitamin D therapy in patients with COPD. Then, publication bias assessment was conducted by funnel plot analysis. Finally, the quality of evidence was assessed by the GRADE system. Results. A total of 15 articles involving 1598 participants were included in this study. The overall results showed a statistical significance of vitamin D therapy in patients with COPD which can significantly improve forced expiratory volume in 1 second (FEV1) (MD: 5.69, 95% CI: 5.01-6.38, P < 0.00001 , I 2 = 51 % ) and FEV1/FVC (SMD:0.49, 95% CI: 0.39-0.60, P < 0.00001 , I 2 = 84 % ); and serum 25 (OH)D (SMD:1.21, 95% CI:1.07-1.34, P < 0.00001 , I 2 = 98 % ) also increase CD3+ Tcells (MD: 6.67, 95% CI: 5.34-8.00, P < 0.00001 , I 2 = 78 % ) and CD4+ T cells (MD: 6.00, 95% CI: 5.01-7.00, P < 0.00001 , I 2 = 65 % ); and T lymphocyte CD4+/CD8+ ratio (MD: 0.41, 95% CI: 0.20-0.61, P = 0.0001 , I 2 = 95 % ) obviously decrease CD8+ Tcells(SMD: -0.83, 95% CI: -1.05- -0.06, P < 0.00001 , I 2 = 82 % ), the times of acute exacerbation (RR: 0.40, 95% CI: 0.28-0.59, P < 0.00001 , I 2 = 0 % ), and COPD assessment test (CAT) score (MD: -3.77, 95% CI: -5.86 - -1.68, P = 0.0004 , I 2 = 79 % ). Conclusions. Our analysis indicated that vitamin D used in patients with COPD could improve the lung function (FEV1 and FEV1/FVC), the serum 25(OH)D, CD3+ T cells, CD4 + T cells, and T lymphocyte CD4+/CD8+ ratio and reduce CD8+ T cells, acute exacerbation, and CAT scores.