Acta Universitatis Medicinalis Anhui

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Anhui Provincial Education Department

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Anhui Medical University

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Weng Jianping

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Editorial Board of Acta Universitatis Medi-cinalis Anhui Meishan Road , Hefei 230032

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ISSN 1000 - 1492

CN 34 - 1065/R

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Completecfbgene deletion inStreptococcusagalactiaeleads to qPCR false negatives: a molecular mechanism study

Wang Xiu; Leng Guiyun; Yang Yunsi; Tang Wei; Zhou Qiang; Yao Jie

DOI: 专辑：医药卫生科技

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abstract:
ObjectiveTo investigate the causes of false negative results in the detection of Streptococcus agalactiaeusing fluorescent quantitative PCR (qPCR) targeting the CAMP factor gene ( cfb), and to perform a comprehensive analysis of the associated molecular mechanisms. MethodsA total of 76 vaginal secretion samples were evaluated using both qPCR based on cfb gene and bacterial culture methods. Four suspicious strains exhibiting negative qPCR results but positive culture findings were identified using matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS), latex agglutination antigen detection, and the CAMP test. Whole genome analysis was conducted utilizing the MGI DNBSEQ-T7 and Nanopore-PromethION 48 sequencing platforms. Phylogenetic and circular evolutionary trees were constructed using the 16S rRNA gene for strain verification. Multilocus sequence typing (MLST) was conducted, and cfb sequences were aligned and analyzed based on spliced sequences and original data. Specific primers targeting the cfbgene were designed for full-length amplification, followed by verification through agarose gel electrophoresis. ResultsThe four strains identified as suspicious were classified as S.agalactiae through MALDI-TOF MS, antigen detection, and 16S rRNA gene analysis, with MLST typing indicating ST862. Phenotypic analysis revealed a negative CAMP test. Whole genome sequence alignment failed to detect the cfb gene or any homologous sequences, and molecular testing confirmed the absence of cfb gene PCR amplification products, thereby confirming its complete deletion. Conclusion This deletion is identified as the molecular mechanism responsible for the false negative qPCR detection of S. agalactiae when targeting this specific gene. It is recommended that the qPCR detection targeting a single cfb gene has limitation, and this may impact clinical diagnosis and treatment decisions. This limitation warrants careful consideration.

The impact of mandibular retrognathism on memory and cognitive function in rats

Li Qingchun; Han Quancheng; Liu Xiaoyu; Wu Tingting

DOI: 专辑：医药卫生科技

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abstract:
ObjectiveTo investigate the impact of mandibular retrognathism on brain function in rats and its potential mechanisms. Method Male SD rats aged 3 to 4 weeks (w) were randomly divided into control group ( n=10) and mandible retrusion (MR) group ( n=30), with the MR group further divided into three subgroups: 1, 2, or 4 weeks, with 10 rats in each subgroup. The MR group used modified metal tubes, which were bonded to the lingual side of the maxillary incisors in rats, forcing the mandible to retract by 2 mm-2.5 mm, thereby achieving the goal of constructing a mandibular retrognathism model; the control group received no interventions. The effects of mandibular retraction on the spatial learning ability and memory ability of rats were explored by behavioral experiments such as Morris water maze, Y maze and new object recognition 1, 2, and 4 weeks after modeling, respectively. Hematoxylin-eosin (HE) and Nissl staining were employed to observe the histomorphological changes in CA1, CA3, and DG regions of hippocampal tissues; Immunohistochemistry was employed to detect the protein expression levels of tropomyosin receptor kinase B (TrkB) in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus. Western blot was used to assess the expression changes in the TrkB/phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway in hippocampal tissue. Quantitative analysis of apoptosis-related proteins in the hippocampus, including Bcl-2-associated X protein (Bax), B-cell lymphoma-2 protein (Bcl-2), and Caspase-3, was conducted using qRT-PCR and Western blot. Results Behavioral experiments showed that rats in the MR group, especially the MR4 w group, were significantly weaker in learning and spatial memory than the control group, MR1 w, and MR2 w（ P＜0.05）. HE staining showed that pyramidal cells in the control group were arranged orderly with regular morphology. In contrast, the MR group exhibited a reduction in the number of cells in the hippocampal CA1, CA3, and dentate gyrus (DG) regions. The cells were sparsely and irregularly arranged, with nuclear condensation and enlarged cellular spaces. Nissl staining further demonstrated damage to the Nissl bodies in the MR group. Meanwhile, the TrkB/PI3K/AKT signaling pathway was activated in the MR group, and the expression of p-TrkB, PI3K, and p-AKT proteins was up-regulated ( P<0.05); Western blot and qRT-PCR indicated that MR up-regulated the expression of pro-apoptotic protein Bax, apoptotic effector protein Caspase-3 ( P<0.05), and inhibited the expression of anti-apoptotic protein Bcl-2 ( P<0.05). Conclusion Mandibular retraction impairs brain function and affects cognition and learning memory in rats. This may be achieved by regulating the TrkB/PI3K/AKT signaling pathway to induce apoptosis in hippocampal neurons.

Effect of vitamin D on NF-κB/CBS-H2S signaling pathway in rats with chronic sciatic nerve injury

Zhang Qin; Jiang Zhongjin; Ao Shengfu

DOI: 专辑：医药卫生科技

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abstract:
Objective To investigate the ameliorative effect of vitamin D on sciatic nerve chronic compression injury (CCI) rats and its regulatory effect on nuclear factor κB (NF-κB)/cystathione-β-synthase (CBS)-hydrogen sulfide (H 2S) system. Methods Fifty rats were randomly divided into five groups: control group, model group, Vitamin D group, activator group, and activator + vitamin D group, with 10 rats in each group. Except for the control group, the rats in the other groups underwent sciatic nerve ligation to establish the CCI model. The vitamin D group received intraperitoneal injection of 500 mg/kg Vitamin D, the activator group received intraperitoneal injection of 10 mg/kg NF-κB activator lipopolysaccharide, and the activator + vitamin D group received intraperitoneal injection of 500 mg/kg vitamin D along with 10 mg/kg lipopolysaccharide. The control and model groups received intraperitoneal injection of an equal volume of saline, once per day for 2 weeks. The following parameters were compared among the groups: paw withdraw thermal latency (PWTL), mechanical withdrawal threshold (MWT), serum 25-hydroxyvitamin D 3 [25(OH)D 3] levels, H2S content, calcitonin gene-related peptide (CGRP), prostaglandin E2 (PGE2) levels, and the expression of vitamin D receptor (VDR), NF-κBp65, and CBS proteins in the L4-L6 dorsal root ganglia of rats. Results Compared with the control group, the model group showed decreased PWTL, MWT, 25(OH)D 3 levels and VDR protein expression, while H 2S content, CGRP and PGE2 levels, and NF-κBp65 and CBS protein expression significantly increased ( P<0.05). Compared with the model group, the vitamin D group exhibited increased PWTL, MWT, 25(OH)D 3 levels and VDR protein expression ( P<0.05), while H 2S content, CGRP and PGE2 levels, and NF-κBp65 and CBS protein expression significantly decreased ( P<0.05). Compared with the activator group, the activator + Vitamin D group showed increased PWTL, MWT, 25(OH)D 3 levels and VDR protein expression, and decreased H 2S content, CGRP and PGE2 levels and decreased NF-κBp65, CBS protein expression ( P<0.05). Compared with the vitamin D group, the activator + vitamin D group showed decreased PWTL, MWT, 25(OH)D 3 levels and VDR protein expression, while H 2S content, CGRP and PGE2 levels, and NF-κBp65 and CBS protein expression significantly increased ( P<0.05). ConclusionExogenous supplementation of vitamin D can relieve nerve pain and reduce pain sensitivity in CCI rats, possibly by inhibiting NF-κB/CBS-H 2S signaling pathway.

Investigation of the impact and mechanism ofIRF2BP2knockdown on the proliferation in acute myeloid leukemia cells

Zhou Bi; Tang Xiaodong; Li Ying; Zhang Yongping; Hu Shaoyan

DOI: 专辑：医药卫生科技

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The mechanism of RACK1 regulating LPS-induced functional damage of rat pulmonary microvascular endothelial cells

Li Qiqi; Wu Xianghui; You Qinghai

DOI: 专辑：医药卫生科技

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Nomogram based on DCE-MRI radiomics combined with clinical-radiological features in predicting hormone receptor status in breast cancer with low Her-2 expression

Hou Weishu; Pan Hongli; Wang Qun; Li Xiaohu; Yan Yunwen; Yu Yongqiang

DOI: 专辑：医药卫生科技

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Icariin inhibits the migration and invasion of triple negative breast cancer by interfering the TFG-β/Smad signalling pathway

Xiao Zengyou; Yang Zean; Chen Caihong; Li Jiaxian; He Yujie; Fu Pinting; Wang Jie

DOI: 专辑：医药卫生科技

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abstract:
Objective To investigate the mechanism by which icariin (ICA) inhibits the invasion and metastasis of human triple-negative breast cancer (TNBC) cells via downregulation of the transforming growth factor-β/Smad (TGF-β/Smad) signaling pathway. M ethodsTNBC cells (MDA-MB-231 and MDA-MB-468) were cultured in vitro and divided into four groups: an experimental group treated with 15 μmol/L ICA; a model group treated with 10 μmol/L TGF-β receptor inhibitor LY2109761; a combination group (LY2109761+ICA) treated with both 15 μmol/L ICA and 10 μmol/L LY2109761; and a control group. Cell proliferation, migration, and invasion were assessed using CCK-8, colony formation, 5-ethynyl-2′-deoxyuridine (EdU), wound healing, and Transwell assays. The expression levels of epithelial-mesenchymal transition (EMT)-related proteins, as well as TGF-β1, Smad2, and phosphorylated Smad2 (P-Smad2) were detected by immunofluorescence and Western blot. ResultsCCK-8 results showed that cell proliferation decreased gradually with increasing concentrations of ICA ( P<0.05). Colony formation and EdU assays indicated significantly inhibited proliferation in the ICA-treated group compared to the control ( P<0.05). Wound healing and Transwell assays demonstrated reduced migration and invasion capabilities in the experimental group relative to the control ( P<0.05). Compared to the model group, the LY2109761+ICA group exhibited further suppression of invasion ( P<0.05). Immunofluorescence revealed decreased Vimentin expression in the experimental group ( P<0.05), with an even more pronounced reduction in the LY2109761+ICA group ( P<0.01). Western blot analysis showed that the protein levels of N-cadherin, matrix metalloproteinase-9 (MMP9), Vimentin, TGF-β1, Smad2, and P-Smad2 were downregulated in the experimental group compared to the control ( P<0.05). These proteins were further suppressed in the LY2109761+ICA group compared to the model group ( P<0.05). ConclusionsICA inhibits TNBC cells proliferation, invasion, metastasis, and EMT by downregulating the TGF-β/Smad signaling pathway.

The Role of STAT3 phosphorylation in regulating ferroptosis and its impact on cisplatin resistance in human osteosarcoma cCells

Wang Xinping; Wang Linkuan; Hu Pengchao; Shi Yihua

DOI: 专辑：医药卫生科技

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abstract:
ObjectiveTo investigate the role of STAT3 phosphorylation in ferroptosis regulation and its impact on cisplatin resistance mechanisms in human osteosarcoma cells. Methods Human osteosarcoma HOS cells and cisplatin-resistant HOS/DDP cells were treated with cisplatin (0.5, 1, 2, 4, 8, 16, 32 mg/L), the ferroptosis inducer Erastin (Era) (2 μmol/L), and/or the ferroptosis inhibitor Ferrostatin-1 (Fer1) (10 μmol/L). Cell viability and proliferation were assessed using the Cell Counting Kit-8 (CCK-8) and colony formation assays, and cell migration was evaluated via a scratch assay. Reactive oxygen species (ROS), intracellular ferrous iron levels, mitochondrial membrane potential, mitochondrial function, malondialdehyde (MDA) levels, and the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio were measured using commercial kits. The mRNA expression of ferroptosis-related genes was analyzed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). The protein levels of glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), phosphorylated STAT3 (p-STAT3), and total STAT3 were determined by Western blot. Results With cisplatin treatment, HOS cells exhibited decreased cell viability, mitochondrial membrane potential, and GSH/GSSG ratio ( P < 0.01), along with elevated levels of ROS, ferrous ion, and MDA content ( P < 0.01). The protein levels of GPX4 ( P < 0.01), SLC7A11, and p-STAT3 also decreased ( P < 0.05). Coadministration with the ferroptosis inhibitor Ferrostatin-1 (Fer-1) reversed these aforementioned effects ( P < 0.05). In HOS/DDP cells, the mRNA levels of ferroptosis-suppressive genes ( GPX4, FTH1, SLC7A11, and AIFM2) were significantly higher than those in HOS cells ( P < 0.05), whereas the expression of ferroptosis-promoting genes ( ACSL4 and PTGS2) was significantly lower ( P < 0.05). The cisplatin-induced reductions in cell viability and mitochondrial membrane potential, as well as the increases in ROS, ferrous ion, and MDA levels, were less pronounced in HOS/DDP cells than in HOS cells. The SLC7A11 protein level showed no significant change. However, combined treatment with the ferroptosis inducer Erastin (Era) resulted in significant decreases in viability, mitochondrial membrane potential, and the GSH/GSSG ratio in HOS/DDP cells ( P < 0.05). Furthermore, the protein levels of p-STAT3, GPX4, and SLC7A11 were also markedly reduced ( P < 0.05). Conclusion The activation of ferroptosis mediated by p-STAT3 enhances cisplatin sensitivity in HOS/DDP cells.

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