المؤلفون: Hong Zhu¹, Dan Ren¹, Lan Xiao¹ LanXiaoLX1103@163.com, Ting Zhang¹, Ruomeng Li¹, Bin Guan¹, Jing Zhang²

المصدر: Tropical Journal of Pharmaceutical Research. Oct2019, Vol. 18 Issue 10, p2037-2043. 7p.

مصطلحات موضوعية: *ANTHOCYANINS, *LACTATE dehydrogenase, *APOPTOSIS, *CELLS, *CELL survival, *CYTOPROTECTION, *BCL-2 proteins

مستخلص: Purpose: To investigate whether the cytoprotective effect of anthocyanin (Anc) on oxygen-glucose deprivation/reperfusion (OGD/R)-induced cell injury is related to apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK)/p38 signaling pathway. Methods: PC12 cells were pre-treated with various concentrations of Anc (10, 50, and 100 μg/mL) in OGD/R-induced cell injury model. The 3-(4, 5)-dimethylthiahiazo (-z-y1)-3, 5-di-phenytetrazoliumromide (MTT) assay was used to assess cell viability. Cell apoptosis was measured by lactic acid dehydrogenase (LDH) release assay and flow cytometry. Western blot was employed to determine the protein expressions of BCL-2, BAX, caspase-3, p-ASK1 (Thr845), p-JNK, and p-p38. Results: The results indicate that Anc increased the viability of PC12 cells after OGD/R exposure (p < 0.05), and also efficiently rescued OGD/R-induced apoptosis (p < 0.05). Mechanistic studies showed that these protective roles of Anc are related to the inhibition of ASK1/JNK/p38 signaling pathway. Conclusion: The results indicate Anc protects against OGD/R-induced cell injury by enhancing cell viability and inhibiting cell apoptosis. The underlying mechanism of action is partly via inactivation of ASK1/JNK/p38 signaling pathway. Thus, Anc has promise as a potential natural agent to prevent and treat cerebral ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

المؤلفون: Zhou, Yuan¹ (AUTHOR), Tao, Pingde¹ (AUTHOR), Wang, Meigui¹ (AUTHOR), Xu, Peng¹ (AUTHOR), Lu, Wei¹ (AUTHOR), Lei, Pan¹ (AUTHOR), You, Qiuyun^1,2 (AUTHOR) 1471@hbtcm.edu.cn

المصدر: European Journal of Medicinal Chemistry. Sep2019, Vol. 177, p105-115. 11p.

مصطلحات موضوعية: *LACTATE dehydrogenase, *CELL cycle, *CANCER cell proliferation, *CANCER cells, *OXYGEN consumption, *TUMOR growth, *CELL proliferation

مستخلص: Human lactate dehydrogenase A (LDHA) plays a critical role in the glycolytic process, making the enzyme an ideal of anti-cancer drug target. Herein, we report the discovery of novel potent LDHA inhibitors by screening an in-house library. The hit-to-lead modification enabled us to identify compound 24c , which inhibited LDHA activity with an EC 50 value of 90 nM, and reduced MiaPaCa-2 cancer cell proliferation with an IC 50 value of 2.1 μM. In line with the in vitro anticancer activity, 24c suppressed the tumor growth at a dose of 10 mg/kg in a MiaPaCa-2 cells xenograft model, but with little effect to the mice weight. Moreover, 24c strongly inhibited MiaPaCa-2 cell colonies formation, induced MiaPaCa-2 cell apoptosis, and arrested MiaPaCa-2 cell cycle at G2 phase. In addition, the mitochondrial bioenergetics analysis suggested that 24c could reprogram cancer cell metabolic pathways from glycolysis to oxidation phosphorylation, which verified by decreasing the extracellular acidification rates and lactate formation, and increasing oxygen consumption rate in cancer cell. All these results indicate 24c is a promising metabolic modulator for the anticancer drug development. Compound 24c exhibited a potent biochemical potency, and in vitro and in vivo anticancer activity. Image 1 • Compound 24c inhibited LDHA with an EC 50 value of 90 nM. • Compound 24c reduced MiaPaCa-2 cell proliferation with an IC 50 value of 2.1 μM. • Compound 24c suppressed tumor growth in a xenograft model. [ABSTRACT FROM AUTHOR]

المؤلفون: Zhou, Bin¹ (AUTHOR), Liu, Hong-Yun² (AUTHOR), Zhu, Bao-Lian³ (AUTHOR), Yue, Ai-Xia¹ (AUTHOR) likexia_y@126.com

المصدر: Journal of Bioenergetics & Biomembranes. Aug2019, Vol. 51 Issue 4, p291-300. 10p.

مصطلحات موضوعية: *LACTATE dehydrogenase, *MITOCHONDRIAL membranes, *APOPTOSIS, *MEMBRANE potential, *CELLS, *CELL survival

مستخلص: To understand the role of microRNA-141 (miR-141) in hypoxia/reoxygenation (H/R)-induced PC12 cell injury via modulation of Keap1/Nrf2 signaling pathway. PC12 cells were divided into Control, H/R, H/R + miR-141 mimics, H/R + NC, H/R + miR-141 inhibitor, H/R + siKeap1 and H/R + miR-141 inhibitors+siKeap1 groups. The expression of miR-141 and Keap1/Nrf2 pathway was measured by qRT-PCR and western blotting, cell viability evaluated by MTT assay while cell apoptosis tested by flow cytometry. Besides, MDA (malondialdehyde), SOD (Super Oxide Dismutase) and LDH (lactate dehydrogenase) levels were determined. DCFH-DA and JC-1 staining were used to measure ROS and mitochondrial membrane potential (MMP) respectively. Compared with Controls, PC12 cells induced by H/R exhibited decreased cell viability and increased cell apoptosis rate, with elevated MDA, LDH and ROS and reduced SOD levels; and meanwhile, MMP and miR-141 expression were declined, whereas cytoplasmic Nrf2 levels were enhanced with the downregulated nuclear Nrf2 level (all P < 0.05). However, these cells treated with miR-141 mimics and siKeap1 showed obvious improvement in H/R-induced cell injury, while miR-141 inhibitors presented significantly aggravated cell injury (both P < 0.05). Besides, siKeap1 can reverse the effect of miRNA-141 inhibitors on aggravating H/R-induced PC12 cell injury. miR-141-mediated Keap1/Nrf2 signaling pathway to promote cell viability, inhibit cell apoptosis and reduce oxidative stress of PC12 cells, thereby alleviating H/R-induced cell injury. [ABSTRACT FROM AUTHOR]

المؤلفون: Yendubé T. Kantati, Magloire K. Kodjo, Benjamin Lefranc, Magali Basille-Dugay, Jérôme Leprince, Messanvi Gbéassor, David Vaudry

مصطلحات موضوعية: Nutritional Composition and Health Benefits of Jujube Fruit, Food Science, Agricultural and Biological Sciences, Life Sciences, Chronic Cerebral Hypoperfusion-Related Neurodegenerative Diseases, Neurology, Neuroscience, Molecular Mechanisms of Synaptic Plasticity and Neurological Disorders, Cellular and Molecular Neuroscience, Neuroprotective Effects, Neuroprotection, In vivo, Viability assay, Pharmacology, Chemistry, Lactate dehydrogenase, Biochemistry, Apoptosis, Neurotoxicity, Biology, Traditional medicine, Toxicity, Medicine, Enzyme, Biotechnology, Organic chemistry

الوصف: Plants are a valuable source of information for pharmacological research and new drug discovery. The present study aimed to evaluate the neuroprotective potential of the leaves of the medicinal plant Sterculia setigera . In vitro , the effect of Sterculia setigera leaves dry hydroethanolic extract (SSE) was tested on cultured cerebellar granule neurons (CGN) survival when exposed to hydrogen peroxide (H 2 O 2 ) or 6-hydroxydopamine (6-OHDA), using the viability probe fluorescein diacetate (FDA), a lactate dehydrogenase (LDH) activity assay, an immunocytochemical staining against Gap 43, and quantification of the expression of genes involved in apoptosis, necrosis or oxidative stress. In vivo , the effect of intraperitoneal (ip) injection of SSE was assessed on the developing brain of 8-day-old Wistar rats exposed to ethanol neurotoxicity by measuring caspase-3 activity on cerebellum homogenates, the expression of some genes in tissue extracts, the thickness of cerebellar cortical layers and motor ... : تعد النباتات المجردة مصدرًا قيمًا للمعلومات للبحوث الدوائية واكتشاف الأدوية الجديدة. هدفت هذه الدراسة إلى تقييم إمكانات الحماية العصبية لأوراق النبات الطبي Sterculia setigera . في المختبر ، تم اختبار تأثير مستخلص الإيثانول المائي الجاف (SSE) على بقاء الخلايا العصبية الحبيبية المخيخية المستزرعة (CGN) عند تعرضها لبيروكسيد الهيدروجين (H 2 O 2 ) أو 6 -هيدروكسيدوبامين (6 - OHDA)، باستخدام اختبار نشاط فلوريسين ثنائي الأسيتات (FDA)، ومقايسة نشاط نازعة هيدروجين اللاكتات (LDH)، وتلطيخ كيميائي مناعي ضد الفجوة 43، وتحديد كمية التعبير عن الجينات المشاركة في موت الخلايا المبرمج أو النخر أو الإجهاد التأكسدي. في الجسم الحي ، تم تقييم تأثير الحقن داخل الصفاق على الدماغ النامي لفئران ويستار البالغة من العمر 8 أيام المعرضة للسمية العصبية للإيثانول عن طريق قياس نشاط كاسباس 3 على متجانسات المخيخ، والتعبير عن بعض الجينات في مستخلصات الأنسجة، وسمك الطبقات القشرية المخيخية والتنسيق الحركي. في المختبر ، قام SSE بحماية CGN ضد H 2 O 2 و 6 - OHDA موت الخلايا المستحث بجرعة 10 ميكروغرام/مل، وتمنع التعبير عن الجينات Casp 3 و Bad ، وأعادت ...

العلاقة: https://dx.doi.org/10.60692/avhwy-r9v57Test

الإتاحة: https://doi.org/10.60692/w45et-84a9810.60692/avhwy-r9v57Test

المؤلفون: Adeyemi Fatai Odetayo, Wale Johnson Adeyemi, Luqman Aribidesi Olayaki

مصطلحات موضوعية: Endocrine Disruption by Chemical Exposure, Health, Toxicology and Mutagenesis, Environmental Science, Physical Sciences, Genotoxicity and Carcinogenesis Mechanisms, Cancer Research, Biochemistry, Genetics and Molecular Biology, Life Sciences, Mechanisms of Estrogen Receptor Signaling, Genetics, FOS Biological sciences, Bisphenol A, Endocrinology, Internal medicine, Testosterone patch, Hormone, Oxidative stress, Lactate dehydrogenase, Apoptosis, Biology, Chemistry, Medicine, Biochemistry, Enzyme

الوصف: Bisphenol F (BPF), an alternative to bisphenol A has been implicated as a gonadotoxic substance. BPF has been shown to induce hormonal imbalance and testicular oxidative damage. However, the mechanism associated with BPF-induced testicular toxicity has not been fully explored. This study was designed to explore the role of tumor protein (p53)/ B-cell lymphoma 2 (BCl-2) signaling and oestrogen receptor beta (Erβ) in BPF-induced testicular toxicity.Male Wistar rats were randomized into control (Cntrl), BPF-treated (10, 30, and 50 mg/kg for low dose (BPF-L), medium dose (BPF-M), and high dose (BPF-H) respectively), and BPF-treated recovery (Cntrl-R, BPF-L-R, BPF-M-R, and BPF-H-R). The administration was via gavage and lasted for 28 days and the animals in the recovery groups were allowed 28-days exposure free period for recovery from BPF exposure.BPF resulted in the distortion of the testicular histoarchitecture, which was accompanied by a significant rise in testicular gamma-lutamyl transferase and lactate ... : يعتبر ثنائي الفينول و (BPF)، وهو بديل لثنائي الفينول أ، مادة سامة للغدد التناسلية. وقد ثبت أن عامل تضخم البروستاتا يسبب اختلال التوازن الهرموني والضرر التأكسدي للخصية. ومع ذلك، لم يتم استكشاف الآلية المرتبطة بتسمم الخصية الناجم عن عامل تضخم البروستاتا بشكل كامل. تم تصميم هذه الدراسة لاستكشاف دور بروتين الورم (ص 53)/سرطان الغدد الليمفاوية للخلايا البائية 2 (BCL -2) وإشارات مستقبلات الاستروجين بيتا (Erβ) في سمية الخصية المستحثة بـ BPF. تم توزيع فئران ويستار الذكور عشوائيًا على السيطرة (Cntrl)، وعلاج BPF (10 و 30 و 50 مجم/كجم للجرعة المنخفضة (BPF - L)، والجرعة المتوسطة (BPF - M)، والجرعة العالية (BPF - H) على التوالي)، والتعافي المعالج بـ BPF (Cntrl - R و BPF - L - R و BPF - M - R و BPF - H - R). تم إعطاء الدواء عن طريق التلقيح الصناعي واستمر لمدة 28 يومًا وتم السماح للحيوانات في مجموعات الاسترداد بفترة خالية من التعرض لمدة 28 يومًا للتعافي من التعرض لعامل تضخم البروستاتا. أدى عامل تضخم البروستاتا إلى تشويه بنية نسيج الخصية، والذي كان مصحوبًا بارتفاع كبير في أنشطة إنزيم جاما لوتاميل للخصية ونازعة هيدروجين ...

العلاقة: https://dx.doi.org/10.60692/09bp1-n4z96Test

الإتاحة: https://doi.org/10.60692/mbkfj-5yd5410.60692/09bp1-n4z96Test

المؤلفون: Çavuşoğlu, T., Gökhan, A., Kiliç, K.D., Şirin, C., Tomruk, C., Yiğittürk, G., Erbaş, O.

مصطلحات موضوعية: cryopreservation, animal experiment, Calcium, ovary, platelet-rich plasma, vitrification, caspase 3, catalase, connexin 43, hydrogel, ketamine, lactate dehydrogenase, malonaldehyde, mitochondrial permeability transition pore, myeloperoxidase, protein bcl 2, angiogenesis, animal model, animal tissue, antibody labeling, apoptosis, Article, astrocyte, biochemical analysis, cell proliferation, cell protection, cell survival, cervical spine dislocation, controlled study, cumulus cell

الوصف: Background/aim: The subject of this study was to investigate the utility of platelet-rich plasma (PRP) in the cryopreservation process to reduce cryodamage and increase tissue viability. Materials and methods: Twenty-one female Wistar rats were randomly allocated to three groups. In Group 1 (G1), rats were not subjected to vitrification (n = 7). Group 2 (G2) was the vitrification group in which PRP was added to the basic vitrification solution (n = 7). Group 3 (G3) was the vitrification group in which fetal bovine serum was added to the basic vitrification solution (n = 7). Warmed tissues were evaluated with histochemical (HC) and immunohistochemical (IHC) staining, the TUNEL method, immunofluorescence (IF) staining, and biochemical analyses. Results: The percentages of IHC staining, TUNEL method positivity, and IF staining were significantly higher in G2 compared to both G1 and G3 (P 0.05). G2 ovaries exhibited a significant increase in both malondialdehyde and catalase values in comparison to G1 (P 0.05). In HC staining, degenerations in primary and secondary follicles and in ovarian tissue were more common in the PRP-supplemented group. The calcium used in PRP activation was suspected to have increased the degeneration and prevented the possible positive effects of PRP. Conclusion: To the best of our knowledge, PRP-supplemented vitrification solution was used for the first time in the literature in this study in whole rat ovarian tissue vitrification. If PRP is to be used as a component in vitrification solution for rat ovarian tissue, the use of lower amounts of calcium or different methods in PRP activation, or the use of nonactivated PRP, should be considered from the beginning. © TÜBİTAK. ; Ege Üniversitesi

العلاقة: Turkish Journal of Medical Sciences; Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı; https://hdl.handle.net/11454/92869Test; https://doi.org/10.55730/1300-0144.5694Test; 53; 1281; 1292

الإتاحة: https://doi.org/10.55730/1300-0144.5694Test
https://hdl.handle.net/11454/92869Test

المؤلفون: Liu, Xinyue, Yang, Yao, Tang, Xuefei, Guo, Li, Tang, Xinhui, Zhu, Ting, Zhao, Tiannan, Zhang, Weina, Zhang, Ping

المصدر: Evidence-based Complementary & Alternative Medicine (eCAM); 10/5/2022, p1-18, 18p, 2 Diagrams, 1 Chart, 6 Graphs

مصطلحات موضوعية: FLOW cytometry, OVARIAN tumors, WESTERN immunoblotting, EPIDERMAL growth factor receptors, CELL receptors, APOPTOSIS, CELLULAR signal transduction, GENE expression, LACTATE dehydrogenase, PLANT extracts, PHARMACEUTICAL chemistry, CELL lines

مستخلص: This study was intended to establish the predictive target of Shikonin (SK) against ovarian cancer using network pharmacology and to clarify the potential mechanism of SK in promoting apoptosis in ovarian cancer. Cell Counting Kit-8 assay, plate clone assays, LDH assay, flow cytometric analysis of Annexin V-fluorescein isothiocyanate/propidium iodide staining, and western blotting were used to assess the effect of SK on apoptosis of ovarian cancer cell lines (SKOV3 and A2780). Pharmacodynamic targets were used to predict the targets of SK and ovarian cancer. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway enrichment analyses were used to analyze the biological functions and signal pathways of these targets. SK promoted apoptosis in ovarian epithelioid adenocarcinoma cells. SK-ovarian cancer pharmacodynamic target analysis screened 17 related genes. GO and KEGG analyses showed that SK affected the estrogen signaling pathway. SK inhibited the expression of GPER in SKOV3 and A2780 cells and downregulated the expression of EGFR, p-EGFR, PI3K, and p-AKT in a concentration-dependent manner. The apoptosis-promoting effect of SK was enhanced by GPER-specific agonist G1 and inhibited by the specific inhibitor G15. The expression of EGFR, p-EGFR, PI3K, and p-AKT was decreased by G1 and reversed by G15. SK also inhibited tumor growth in the SKOV3 xenograft model, and it acted synergistically with G1. However, the effect can be attenuated by G15 in vivo. In summary, SK may affect the apoptosis of ovarian cancer cells through GPER/EGFR/PI3K/AKT, and GPER may be a key target of SK in ovarian cancer cell apoptosis. [ABSTRACT FROM AUTHOR]

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المؤلفون: Li, Yang, Wen, Cheng, Zhong, Jialin, Ling, Junqi, Jiang, Qianzhou

المصدر: Oral Diseases; Oct2022, Vol. 28 Issue 7, p2026-2035, 10p, 2 Color Photographs, 4 Graphs

مصطلحات موضوعية: ENTEROCOCCAL infections, FLOW cytometry, ENTEROCOCCUS faecium, PERIODONTITIS, WESTERN immunoblotting, APOPTOSIS, OSTEOBLASTS, INTERLEUKIN-1, LACTATE dehydrogenase, CELL lines, CASPASES, MEMBRANE potential

مستخلص: Objective: Regulated cell death is key in the pathogenesis of persistent apical periodontitis. Here, we investigated the mechanisms of regulated cell death in osteoblast‐like MG63 cells infected with Enterococcus faecalis OG1RF. Materials and methods: MG63 cells were infected with live E. faecalis OG1RF at the indicated multiplicity of infection for the indicated infection time. We evaluated the cells by flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labelling assay and lactate dehydrogenase release analysis; measured the activity of caspase‐1/‐3/‐8/‐9 and the release of interleukin‐1β; and determined the expression of apoptosis‐associated proteins and gasdermin D by apoptosis antibody array and Western blotting. Results: Enterococcus faecalis OG1RF reduced the mitochondrial membrane potential of the infected cells, increased the percentage of apoptotic and terminal deoxynucleotidyl transferase dUTP nick end labelling‐positive cells, and enhanced lactate dehydrogenase release. The expression of caspase‐3 and survivin and the activity of caspase‐3/‐8/‐9 were upregulated, while the expression of death receptor 6 was downregulated. The activity of caspase‐1/gasdermin D and the release of interleukin‐1β remained unaltered. Conclusion: Enterococcus faecalis OG1RF induced both intrinsic and extrinsic MG63 cell apoptosis via caspase‐3/‐8/‐9 activation but did not activate the pyroptotic pathway regulated by caspase‐1/gasdermin D. [ABSTRACT FROM AUTHOR]

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المؤلفون: Son, Seogho, Yoo, Seung-ah, Nam, KeeSoo, Oh, Sunhwa, Lee, Kyung-min, Yi, Jae Youn, Shin, Incheol

المصدر: Animal Cells & Systems; Oct2022, Vol. 26 Issue 5, p203-213, 11p

مصطلحات موضوعية: CREATINE kinase, BREAST cancer, SMAD proteins, CELL cycle, LACTATE dehydrogenase, CANCER cells, DOXORUBICIN

مستخلص: Brain type of creatine kinase (CKB) regulates energy homeostasis by reversibly transferring phosphate groups between phosphocreatine and ATP at sites of high energy demand. Several types of cancer cells exhibit upregulated CKB expression, but the function of CKB in cancer cells remains unclear. In this study, we investigated the function of CKB in breast cancer by overexpressing CKB in MDA-MB-231 cells. The overexpression of CKB did not affect cell growth rate, cell cycle distribution, ATP level or key mediators of aerobic glycolysis and lactate dehydrogenase isoform levels. Meanwhile, CKB overexpression did increase resistance to doxorubicin. TGF-β-induced Smad phosphorylation and Smad-dependent transcriptional activity were significantly up-regulated by CKB expression without changes in inhibitory Smad protein levels. Moreover, treatment with TGF-β considerably enhanced cell viability during doxorubicin treatment and decreased doxorubicin-induced apoptosis in CKB-expressing MDA-MB-231 cells compared to control cells. These results suggest that CKB attenuates doxorubicin-induced apoptosis and potentiates resistance to doxorubicin by enhancing TGF-β signaling in MDA-MB-231 cells. [ABSTRACT FROM AUTHOR]

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المؤلفون: Xu, Weicai, Li, Xiaojun, Chen, Long, Luo, Xiaopan, Shen, Sheliang, Wang, Jing

المصدر: BMC Anesthesiology; 9/26/2022, Vol. 22 Issue 1, p1-12, 12p

مصطلحات موضوعية: NEUROTOXICOLOGY, FLOW cytometry, REVERSE transcriptase polymerase chain reaction, ROPIVACAINE, SYNDROMES, NEURONS, NEUROBLASTOMA, ANIMAL experimentation, WESTERN immunoblotting, APOPTOSIS, MICRORNA, IMIDAZOLES, GENE expression, CELL survival, CELL proliferation, LACTATE dehydrogenase, BRAIN-derived neurotrophic factor, MICE

مستخلص: Background: Ropivacaine is commonly applied for local anesthesia and may cause neurotoxicity. Dexmedetomidine (DEX) exhibits neuroprotective effects on multiple neurological disorders. This study investigated the mechanism of DEX pretreatment in ropivacaine-induced neurotoxicity. Methods: Mouse hippocampal neuronal cells (HT22) and human neuroblastoma cells (SH-SY5Y) were treated with 0.5 mM, 1 mM, 2.5 mM, and 5 mM ropivacaine. Then the cells were pretreated with different concentrations of DEX (0.01 μM, 0.1 μM, 1 μM, 10 μM, and 100 μM) before ropivacaine treatment. Proliferative activity of cells, lactate dehydrogenase (LDH) release, and apoptosis rate were measured using CCK-8 assay, LDH detection kit, and flow cytometry, respectively. miR-10b-5p and BDNF expressions were determined using RT-qPCR or Western blot. The binding of miR-10b-5p and BDNF was validated using dual-luciferase assay. Functional rescue experiments were conducted to verify the role of miR-10b-5p and BDNF in the protective mechanism of DEX on ropivacaine-induced neurotoxicity. Results: Treatment of HT22 or SH-SY5Y cells with ropivacaine led to the increased miR-10b-5p expression (about 1.7 times), decreased BDNF expression (about 2.2 times), reduced cell viability (about 2.5 times), elevated intracellular LDH level (about 2.0–2.5 times), and enhanced apoptosis rate (about 3.0–4.0 times). DEX pretreatment relieved ropivacaine-induced neurotoxicity, as evidenced by enhanced cell viability (about 1.7–2.0 times), reduced LDH release (about 1.7–1.8 times), and suppressed apoptosis rate (about 1.8–1.9 times). DEX pretreatment repressed miR-10b-5p expression (about 2.5 times). miR-10b-5p targeted BDNF. miR-10b-5p overexpression or BDNF silencing reversed the protective effect of DEX pretreatment on ropivacaine-induced neurotoxicity, manifested as reduced cell viability (about 1.3–1.6 times), increased intracellular LDH level (about 1.4–1.7 times), and elevated apoptosis rate (about 1.4–1.6 times). Conclusions: DEX pretreatment elevated BDNF expression by reducing miR-10b-5p expression, thereby alleviating ropivacaine-induced neurotoxicity. [ABSTRACT FROM AUTHOR]

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