Chinese Journal of Biochemistry and Molecular Biology-Channel: Research Papers Channel: Research Papers http://cjbmb.bjmu.edu.cn EN-US http://cjbmb.bjmu.edu.cn/EN/current.shtml http://cjbmb.bjmu.edu.cn 5 <![CDATA[Preparation and Identification of Sulfadimethoxine Nanobody Immunomagnetic Beads]]> E. coli BL21 (DE3) for expression, respectively. Then, Nb-(G4S)1-Cys and Nb-(G4S)4-Cys were conjugated with BMPs using N-succinimidyl-3-(2-pyridyldithiol)propionate (SPDP). The coupling was verified by Western blot, and the coupling conditions were optimized. The hydrated particle size, Zeta potential, and dispersibility of the immunomagnetic beads were analyzed by transmission electron microscopy and Zeta potential analyzer. The results demonstrated that Nb-(G4S)1-Cys and Nb-(G4S)4-Cys could be immobilized on the surface of BMPs. The coupling efficiency of Nb-(G4S)1-Cys and BMPs was higher than that of Nb-(G4S)4-Cys and BMPs. Characterization revealed that BMP-(G4S)1-Nb exhibited a higher absolute value of Zeta potential, smaller hydrated particle size, and lower polydispersibility index, indicating enhanced colloidal stability in aqueous systems. Taken together, the immunomagnetic beads constructed with BMPs and Nb-(G4S)1-Cys showed better performance than those constructed with BMPs and Nb-(G4S)4-Cys. This study provides theoretical support for the selection of appropriate linker lengths in the construction of efficient immunomagnetic beads for the separation and analysis of SDM pollutants.]]> <![CDATA[Dimethyl Fumarate Alleviates Oxidative Damage of Fine Particulate Matter to the Placenta of Female Rats through the Nrf2/HO-1 Signaling Pathway]]> 2.5 may increase the risk of pregnancy complications and adverse pregnancy outcomes. The aim of this study is to investigate the damage of PM2.5 exposure before pregnancy to the placenta of rats and the underlying regulatory mechanism of dimethyl fumarate (DMF). Forty 6-week-old SPF grade female SD rats were randomly divided into the control group (normal saline), the low-dose PM2.5 group (1.5 mg/kg PM2.5), the high-dose PM2.5 group (7.5 mg/kg PM2.5), a DMF control group (normal saline + 50 mg/kg DMF), and the DMF intervention group (7.5 mg/kg PM2.5 + 50 mg/kg DMF). Rats were exposed to PM2.5 once every two days for a total of a 40 day period. After exposure to PM2.5, the number and average body length of fetuses in the high-dose PM2.5 group were significantly lower than those in the control group (P < 0.05), as well as the activity of superoxide dismutase (SOD), total antioxidant capacity (T-AOC) and the concentration of interleukin-10 (IL-10) in placental tissues in the high-dose PM2.5 group were significantly lower than those in the control group (P < 0.05), while the content of malondialdehyde (MDA) was higher than that in the control group (P < 0.05). After the DMF treatment, the T-AOC in the DMF intervention group was significantly higher than that in the high-dose PM2.5 group (P < 0.01), this suggested that DMF treatment might alleviate the oxidative damage induced by PM2.5. The H&E staining results of rat placental tissues showed that there was a varying degree of reduction in the number of blood cells in the labyrinthine area of the PM2.5 exposure group. The high-dose PM2.5 group had unclear vascular choroids, while the DMF intervention group had a significant increase in the number of blood cells in the labyrinthine area of the placenta and had clear vascular choroids. Western blotting results showed that the protein levels of nuclear factor E2 related factor (Nrf2) and heme oxygenase-1 (HO-1) in the low-dose PM2.5 group and high-dose PM2.5 group were lower than those in the control group (P < 0.01). Compared with the high-dose PM2.5 group, the protein level of Nrf2 and HO-1 in the DMF intervention group was significantly increased (P < 0.05). In summary, DMF may alleviate the oxidative damage to the placenta caused by PM2.5 exposure before pregnancy and improve the body antioxidant capacity through the Nrf2/HO-1 signaling pathway.]]> <![CDATA[Synergistic Effects of TNF-α and VEGF on mESC-Derived Endothelial Progenitor Cells in Promoting Wound Healing]]> in vivo delivery of EPC is inefficient and can impair cell viability and function, thereby affecting therapeutic efficacy. Therefore, it is necessary to improve the biological functions of EPC to promote wound healing. This study induced the generation of CD133+ CD34+ EPC from mouse embryonic stem cells (mESCs) under the influence of 10 ng/mL Vascular Endothelial Growth Factor (VEGF) and 5 ng/mL basic Fibroblast Growth Factor (bFGF). We used mESC-derived EPC as the research object, and applied exogenous tumor necrosis factor-α (TNF-α) and Vascular Endothelial Growth Factor (VEGF) to mESC-EPC. The results showed that the co-treatment with 10 ng/mL TNF-α and 10 ng/mL VEGF significantly promoted the adhesion, cell migration, and luminal formation abilities of EPC compared to the single-factor treatment (P < 0.01). Further, using a murine full-thickness skin wound model, local administration of 10 ng/mL TNF-α and 10 ng/mL VEGF in conjunction with EPC treatment markedly accelerated wound closure (P < 0.05), thickened the dermal layer of the regenerated skin (P < 0.001), and promoted the maturation of the capillary network formed by CD31+ endothelial cells mediated by angiopoietin ANG1 and ANG2. As wound healing progressed, the expression of the pro-inflammatory factor TNF-α was down-regulated (13 days after surgery, the relative expression levels of TNF-α in PBS group, EPC group, VE group, TE group and VTE group were 0.73± 0.01, 0.60 ± 0.02, 0.42 ± 0.02, 0.36 ± 0.01, 0.34 ± 0.03, respectively), creating a conducive inflammatory microenvironment for wound healing. In summary, the synergistic effects of 10 ng/mL TNF-α and 10 ng/mL VEGF enhance the biological functions of EPC, as well as accelerate wound closure and tissue remodeling in mouse skins by promoting new angiogenesis and early inflammatory responses. This offers new insights into celluiar intervions for wound healing therapies.]]> <![CDATA[Efficient Degradation of Variant SARS-CoV-2 S Proteins by ASP<sub>NJ</sub> and Analysis of Biochemical Characteristics of Variant S Proteins]]> Neanthes japonica, pI 4.4 (ASPNJ) could efficiently degrade the S protein of omicron variant strains BA.2, BF.7 and XBB.1, whereas the mutation S proteins obtained stronger resistance to ASPNJ digestion. Preliminary experiments showed that ASPNJ may reduce the pseudovirus infection into 293T-ACE2. ASPNJ can widely and efficiently degrade the S protein. Thus, our results suggested that ASPNJ may become a new tool enzyme for studying the structure and function of SARS-CoV-2.]]> <![CDATA[miR-485-5p Inhibits the Proliferation, Migration and Invasion of Prostate Cancer Cells by Targeting OGT]]> O-linked N-acetylglucosamine transferase (OGT) is a direct target of miR-485-5p. Further examination showed that OGT was highly expressed in prostate cancer, and transfection with OGT siRNA could significantly inhibit the proliferation, migration and invasion of prostate cancer cells and could effectively reverse the effect of miR-485-5p inhibitor. In summary, miR-485-5p can inhibit the proliferation, migration and invasion of prostate cancer cells by negatively regulating OGT.The results of this study are helpful to further elucidate the role and mechanism of miR-485-5p in the development and development of prostate cancer, and can provide experimental basis for searching for therapeutic targets of prostate cancer.]]>