Turkish journal of biology = Turk biyoloji dergisi最新文献

Background/aim: The cross-kingdom biofilm structure formed by Candida tropicalis and Streptococcus mutans may increase caries formation. The aim of this study was to evaluate the in vitro effect of the exogenous tyrosol on single- and dual-species biofilms as well as planktonic cultures formed by C. tropicalis and S. mutans.

Materials and methods: The antimicrobial efficacy of tyrosol was evaluated through broth microdilution, colony-forming unit (CFU) enumeration, and XTT reduction tests to assess cell viability and metabolic activity. Transmission electron microscopy (TEM) was used to examine ultrastructural changes in planktonic cells. Biofilm dynamics were visualized via scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM). The in vitro cytotoxicity of tyrosol was evaluated using NIH/3T3 fibroblast cells.

Results: XTT results showed that the biofilm-reducing effect of amphotericin B (AMB) on single C. tropicalis biofilm at the minimum inhibitory concentration (MIC) and 2× MIC was significantly higher than that of control (47% and 48%, respectively) (p < 0.05). Tyrosol also had a metabolic activity-reducing effect on single C. tropicalis biofilm, but this effect was not statistically significant (39% at 2× MIC and 42% at MIC). Tyrosol and ampicillin (AMP) had no significant reducing effect on single S. mutans biofilm cells (p > 0.05). However, AMP resistance increased in dual culture. CFU enumeration, TEM, SEM, and CLSM data supported these findings. The effect of tyrosol on NIH/3T3 fibroblast cells was suppressive at low concentrations (1-4 mg/mL) and enhancing at high concentrations (4.5-20 mg/mL).

Conclusion: This study investigated the antimicrobial and antibiofilm properties of tyrosol against C. tropicalis and S. mutans, individually and in combination. The results showed that tyrosol inhibited growth and biofilm formation, particularly in dual-species biofilms. Although S. mutans had greater resistance, overall microbial viability was reduced. Despite some observed increase in AMP resistance, tyrosol was selectively cytotoxic, indicating its promise as a natural therapeutic agent pending further research.

Background/aim: Acute myeloid leukemia (AML) is a malignant neoplasm arising from bone marrow hematopoietic stem cells. It is a common subtype of childhood leukemia and remains challenging to cure. Emerging evidence suggests that circular RNAs (circRNAs), a class of noncoding RNAs, play key regulatory roles in tumor biology. Among their various functions, circRNAs often act as 'sponges' for microRNAs (miRNAs), modulating gene expression posttranscriptionally. This study investigates the functional role and clinical relevance of hsa_circ_0001776 in AML.

Materials and methods: Three AML cell lines and 22 peripheral blood samples were analyzed. Differential expression analysis of circRNAs in a GSE dataset was performed to identify significantly down- and upregulated candidates, with thresholds set at logFC less than -1 and p < 0.05 for downregulation, and logFC more than 1 and p < 0.05 for upregulation. The back-splice junction of hsa_circ_0001776 was validated using Sanger sequencing. Its circular nature and stability were confirmed via actinomycin D treatment and RNase R digestion. Quantitative real-time PCR (qRT-PCR) was used to measure circRNA levels in clinical AML samples. The functional effects of hsa_circ_0001776 on proliferation and cell cycle progression were evaluated using the CCK-8 assay and flow cytometry. Bioinformatics analyses predicted putative miRNA interactions, which were validated by dual luciferase reporter assays. A p-value less than 0.05 was considered statistically significant.

Results: hsa_circ_0001776 expression was significantly reduced in AML samples. Overexpression of hsa_circ_0001776 inhibited cell proliferation and induced G1 phase arrest in AML cells, whereas knockdown of hsa_circ_0001776 accelerated cell cycle progression and promoted malignant proliferation. hsa_circ_0001776 was shown to interact with miR-1269b, the pair being negatively correlated. PTEN was identified as a direct downstream target of miR-1269b, with complementary binding sites confirmed by luciferase assays.

Conclusion: hsa_circ_0001776 suppresses AML progression via the miR-1269b/PTEN axis. These findings suggest that hsa_circ_0001776 may serve as a potential diagnostic biomarker and therapeutic target for AML.

Aim: Neuronal cell death plays a critical role in the development of neurological disorders associated with aging. This study aimed to evaluate the beneficial effects of heat-ki lled lactic acid bacteria (hkLAB) on neuroblastoma cells and Caenorhabditis elegans.

Materials and methods: We pretreated heat-killed Lactobacillus fermentum CNU384 (hkCNU384), L. brevis CNU386 (hkCNU386), L. helveticus CNU395 (hkCNU395), and L. paracasei CNU396 (hkCNU396) at a concentration of 10⁹ CFU/mL to investigate their neuroprotective effects on glutamate-induced SH-SY5Y cells and their impact on the lifespan of 6-hydroxydopamine (6-OHDA)-induced C. elegans.

Results: Our findings indicate that hkCNU395 and hkCNU396 protected against glutamate-induced cell death via modulation of the Bax/Bcl-2 apoptosis regulator ratio and enhancement of endogenous antioxidant enzyme activity. Moreover, hkCNU396 significantly improves survival rates in C. elegans with neuron degeneration induced by 6-OHDA.

Conclusion: These results highlight hkCNU396 as a promising paraprobiotic candidate for patients suffering from degenerative neurodegenerative diseases.

Microplastics (MPs) are plastic particles of anthropogenic origin with a size range of 1-5000 μm. Marine MP pollution is increasingly recognized as a significant global environmental challenge. MPs, which enter marine ecosystems from land- and marine-based sources, pose physical, chemical, and biological risks due to the adsorption of various pollutants and the formation of biofilm layers. MPs are found in various organisms from lower to higher trophic levels of the marine food web. The negative effects of MPs on marine organisms depend on their abundance, their characteristics, and the exposure time of organisms to MPs. MPs can adversely affect various vital functions of marine organisms, including survival rate, photosynthesis, growth rate, body composition, reproduction, feeding, and mobility. This review presents the major sources of MPs in the marine environment, as well as their quantities and characteristics. In addition, studies focusing on the potential of MPs to adsorb and transport pollutants, and the levels of accumulation observed in marine organisms, are evaluated. Finally, the responsibilities of stakeholders in mitigating marine MP pollution to maintain marine ecosystem health are discussed. This paper provides a comprehensive review of marine MP pollution, highlighting the main sources of MPs, the pathways through which MPs enter marine ecosystems, the interactions of MPs with coexisting pollutants, their abundance and characteristics in marine organisms, the negative effects of MPs on various marine organisms, and the roles of stakeholders in mitigating MP pollution.

Background: Abdominal aortic aneurysm (AAA), a gradual segmental dilatation of the abdominal aorta, is associated with a high mortality rate. The pathophysiological molecular mechanisms underlying AAA remain unclear. In recent years, changes in miRNA levels have been reported to be involved in the development and treatment of AAA. This study aimed to investigate the potential targets and underlying mechanisms of miR-9-5p in attenuating AAA progression by modulating the inflammatory response.

Materials and methods: Biochemical kits were used to measure the levels of inflammatory factors, antioxidant enzyme activity, and serum oxidative stress in normal and AAA model mice. miR-9-5p overexpression was achieved by transfecting miR-9-5p mimics into CD4⁺ T cells and administering an miR-9-5p agomir to the mice. The effect of miR-9-5p overexpression was evaluated by detecting the expression level of miR-9-5p in CD4⁺ T cells through qRT-PCR. The NF-κB/Nrf2 pathway levels were assessed using immunofluorescence, western blotting, and quantitative PCR. miR-9-5p expression was modulated by transfecting either miR-9-5p mimics or inhibitors, and the impact on CD4⁺IL-10⁺ T-cell differentiation was analyzed using flow cytometry.

Results: Compared with that in the control group, miR-9-5p expression in CD4⁺ T cells from the peripheral blood of AAA model mice was decreased by 28%. In vivo, miR-9-5p intervention reduced AAA formation in model mice and markedly decreased serum oxidative stress damage and inflammatory factor levels. Furthermore, miR-9-5p intervention significantly increased miR-9-5p levels in CD4⁺ T cells both in vitro and in vivo, increased the proportion of CD4⁺IL-10⁺ T cells, suppressed NF-κB expression, and upregulated Nrf2 and its downstream antioxidant genes. Conversely, these therapeutic effects were abolished when an miR-9-5p inhibitor was administered.

Conclusions: By controlling the interaction between the Nrf2 and NF-κB signaling pathways, miR-9-5p mediates the differentiation of CD4⁺IL-10⁺ T cells and alleviates the development of AAA.

Background/aim: The present study investigates the role of Shenfu injection in the treatment of yang-deficient chronic heart failure (CHF).

Materials and methods: Sprague-Dawley (SD) rats were modeled for yang-deficient CHF by abdominal aortic coarctation. Echocardiography was performed to detect changes in cardiac function, and serum N-terminal B-type natriuretic peptide proteins (NT-proBNP), cardiac troponin I (cTnI), and ferroptosis-related factors were measured using ELISA kits. Pathological changes in cardiac tissues were observed through hematoxylin-eosin (HE) and Masson' trichrome staining, cardiomyocyte apoptosis was measured by TUNEL staining, and reactive oxygen species (ROS) production was determined through dihydroethidium (DHE) staining. The expression of nuclear factor E2-related factor 2 (Nrf2), cyclooxygenase 2 (Ptgs2), glutathione peroxidase 4 (GPX4), solute carrier family 3 member 2 (SLC3A2), solute carrier family 7 member 11 (SLC7A11), and acyl-CoA synthetase long-chain family member 4 (ACSL4) in cardiac tissues were analyzed through RT-qPCR. Phosphorylated Akt (p-Akt), phosphorylated GSK-3β (p-GSK-3β), and Nrf2 expression in tissues were tested through immunohistochemistry. The protein expression of the Akt/GSK-3β/Nrf2 pathway was detected by Western blot. The Akt/GSK-3β/Nrf2 pathway inhibitor LY294002 was applied to the rats administrated with Shenfu injection.

Results: Shenfu injection decreased the left ventricular end-diastolic diameter and left ventricular end-systole diameter and increased the left ventricular ejection fraction and left ventricular fractional shortening in rats with CHF. The treatment reduced NT-proBNP and cTnI levels, while improving pathological damage in the cardiac tissue. The treatment was also noted to decrease serum MDA, ACSL4, and Fe²⁺ and increase GSH, GPX4, SOD, and SLC3A2 in the sample; increase GPX4,SLC7A11 and SLC3A2 mRNA in cardiac tissues, and decrease Ptgs2 and ACSL4 mRNA. Shenfu injection was also noted to activate the Akt/GSK-3β/Nrf2 signaling pathway, while LY294002 weakened the therapeutic effect of the treatment on cardiac tissue damage.

Conclusion: Shenfu injection activates the Akt/GSK-3β/Nrf2 pathway to prevent myocardial injury and ferroptosis in yang-deficient CHF.

Background/aim: Tau protein, which is crucial for sustaining the cytoskeletal network by assisting microtubule construction, contributes significantly to the pathophysiology of Alzheimer's disease (AD). The hyperphosphorylation of tau causes it to detach from microtubules (MTs), leading to the formation of neurofibrillary tangles (NFTs) in neurons, which ultimately results in cell death. Thionine (TH), a cationic phenothiazine-structured compound, has been the topic of extensive research due to its interesting physicochemical properties. It is a common biological dye, especially useful in histology due to its strong affinity for biological membranes. Furthermore, TH serves as a photosensitizer in phototherapy. It has a phenothiazine pharmacophore, which makes it selective against microbial and tumor cells. Our prior studies demonstrated that TH inhibits human plasma butyrylcholinesterase (BChE) by acting as a nonlinear inhibitor and also affects amyloid precursor protein (APP) metabolism in PS70 cells. In the current research, we investigated whether TH modulates the phosphorylation of tau in N2a/APPSwe cells.

Materials and methods: Using flow cytometry, we identified the dose range and treatment time of TH that did not affect the viability of N2a/APPSwe cells. The western blot method was used to investigate the effects of TH on total tau and four key tau phosphorylation sites.

Results: The results indicated that TH reduces tau phosphorylation at residues Ser202/Thr205, Ser396, Ser396/Ser404, and Thr181, which contribute to NFT formation.

Conclusion: When all these findings are evaluated together, TH may have a therapeutic potential against AD.

Background/aim: A number of carbonic anhydrase (CA) family proteins have been implicated in cancer. They contribute to the hypoxic microenvironment. CAVII is often downregulated in colorectal carcinoma and it has been associated with increased tumor size, node metastasis, and adverse clinical outcomes. In this study, we aimed to investigate the effect of hypoxia on CAVII protein in human colon cancer and prostate cancer cells. In addition, the regulation of CAH genes in Caenorhabditis elegans was examined. These are homologous to CAVII in humans.

Materials and methods: CAVII expression was analyzed in different cell lines such as human colon cancer (SW480 and HT-29), human prostate cancer (PC3 and LNCaP), human hepatocellular carcinoma (Hep3B) and Human umbilical vein endothelial cells (HUVEC). HT-29 and LNCaP cell lines were subjected to a chemical hypoxia model with CoCl₂. Real-time PCR was used for CAVII mRNA analysis. Western blot and immunofluorescence (IF) staining were used to detect the CAVII protein. The response of CAH genes was also studied at the mRNA level in a chemical hypoxia model with sodium sulfite in C. elegans. CAVII and CAVII-like genes CAH-3, CAH-4, and CAH-5 were analyzed bioinformatically.

Results: We found that CAVII expression decreased under hypoxic conditions in HT-29, but conversely, increased in LNCaP cells at the mRNA and protein level. In the hypoxia model in C. elegans, CAH genes were downregulated. According to bioinformatics analyses, human CAVII was most similar to CAH-3 (98%).

Conclusion: The results emphasize the necessity of addressing hypoxic regulation in different cell and organism groups in cancer and healthy conditions for CA family members that change under physiological and pathophysiological conditions. Postgenomic studies are important to better understand the evolution of these ancient enzymes.

Background/aim: Kabasura kudineer choornam (KKC) is a polyherbal formulation of 15 ingredients. It has antiinflammatory and antimicrobial properties and are effective in managing the symptoms of H1N1 swine flu and COVID-19. However, its mechanism of action is not fully understood. In this study, we examined the effect of KKC on the polarization and function of primary human macrophages.

Materials and methods: Human monocyte-derived macrophages (M0 macrophages) pretreated with KKC extract were polarized into M1, M2a, or M2c subtypes. The expression of the M1/M2 polarization markers was analyzed using qPCR, flow cytometry, and ELISA, and the phagocytosis capacity of macrophages was analyzed using flow cytometry.

Results: Our data show that the KKC treatment increased the expression of the M1 markers IDO1, IL-1β, IL-12a (p35), and TNF in both polarized and unpolarized macrophages at mRNA level. However, it decreased the secretion of IL-12 (p70) in M1 macrophages and increased the secretion of TNF in M0, M2a, and M2c macrophages. IL-10 secretion was increased in M0 and M2a macrophages, while it was decreased in M1 macrophages after the KKC treatment. Interestingly, all KKC-treated macrophage phenotypes displayed a downregulation in the expression of the M1/M2 surface markers CD64, CD206, CD209, and CD163, which also play a role in phagocytosis. In accordance with this result, the phagocytic capacity of both polarized and unpolarized macrophages was decreased after the KKC treatment.

Conclusion: KKC extract modulates macrophage inflammatory response and could be a potential supplement for the treatment of infectious and inflammatory diseases.