In vitro effects of Zinc in soluble and homeopathic formulations on macrophages and astrocytes

Homeopathy ◽  
2017 ◽  
Vol 106 (02) ◽  
pp. 103-113 ◽  
Author(s):  
Clara Bonafini ◽  
Marta Marzotto ◽  
Paolo Bellavite
Keyword(s):  
Nitric Oxide ◽  
Cell Viability ◽  
Soluble Form ◽  
Enzyme Linked Immunosorbent Assay ◽  
Therapeutic Effects ◽  
Experimental Conditions ◽  
Nitric Oxide Release ◽  
Tnf Α ◽  
High Zinc ◽  
Zinc Depletion

Zinc is an important metal in body homeostasis. Zinc in soluble form (Zn2+) and homeopathic Zincum metallicum were tested in macrophages and astrocytes in order to investigate its potential toxic or therapeutic effects. We evaluated cell viability (WST assay), cytokine production such as tumour necrosis factor alpha (TNF-α) and interleukin 10 (IL-10) by enzyme-linked immunosorbent assay (ELISA) and nitric oxide release by Griess reaction. The effect of zinc-depletion and high zinc pre-treatments on the cell adaptation capability was also investigated. In THP-1 macrophage cell line and in human primary macrophages, Zn2+ at sub-toxic doses (30 μM) caused stimulation of TNF-α and IL-10 with different dynamics reaching the maximum peak at the zinc concentration 100 μM, before the cell death. Highest doses (300 μM) impaired dramatically cell vitality. Similar effects on cell viability were obtained also in C6 astrocytes, where Zn2+ slightly increased the nitric oxide release only in cells activated by one of the pro-inflammatory stimuli used in our cellular model (interferon gamma plus TNF-α). Zinc depletion markedly reduced IL-10 production and cell viability. Zincum metallicum did not cause toxicity in any cell type and showed some small stimulation in WST assay that was statistically significant in a few experimental conditions.

scholarly journals Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3573
Author(s):  
Lian-Chun Li ◽  
Zheng-Hong Pan ◽  
De-Sheng Ning ◽  
Yu-Xia Fu
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathway ◽  
Morphological Changes ◽  
Raw264.7 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

scholarly journals Development of Injectable Polydactyly-Derived Chondrocyte Sheets

2021 ◽  
Vol 22 (6) ◽  
pp. 3198
Author(s):  
Shiho Wasai ◽  
Eriko Toyoda ◽  
Takumi Takahashi ◽  
Miki Maehara ◽  
Eri Okada ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cartilage Damage ◽  
Enzyme Linked Immunosorbent Assay ◽  
Invasive Treatment ◽  
Experimental Conditions ◽  
Humoral Factors ◽  
Less Invasive ◽  
Cell Counts ◽  
Invasive Method ◽  
Injection Control

We are conducting a clinical study of the use of allogeneic polydactyly-derived chondrocyte sheets (PD sheets) for the repair of articular cartilage damage caused by osteoarthritis. However, the transplantation of PD sheets requires highly invasive surgery. To establish a less invasive treatment, we are currently developing injectable fragments of PD sheets (PD sheets-mini). Polydactyly-derived chondrocytes were seeded in RepCell™ or conventional temperature-responsive inserts and cultured. Cell counts and viability, histology, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qPCR), and flow cytometry were used to characterize PD sheets-mini and PD sheets collected from each culture. To examine the effects of injection on cell viability, PD sheets-mini were tested in four experimental conditions: non-injection control, 18 gauge (G) needle, 23G needle, and syringe only. PD sheets-mini produced similar amounts of humoral factors as PD sheets. No histological differences were observed between PD sheets and PD sheets-mini. Except for COL2A1, expression of cartilage-related genes did not differ between the two types of PD sheet. No significant differences were observed between injection conditions. PD sheets-mini have characteristics that resemble PD sheets. The cell viability of PD sheets-mini was not significantly affected by needle gauge size. Intra-articular injection may be a feasible, less invasive method to transplant PD sheets-mini.

scholarly journals Differential Induction of the Toll-Like Receptor 4-MyD88-Dependent and -Independent Signaling Pathways by Endotoxins

2005 ◽  
Vol 73 (5) ◽  
pp. 2940-2950 ◽  
Author(s):  
Susu M. Zughaier ◽  
Shanta M. Zimmer ◽  
Anup Datta ◽  
Russell W. Carlson ◽  
David S. Stephens
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Lipid A ◽  
Raw 264.7 ◽  
Receptor Complex ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nitric Oxide Release ◽  
Tnf Α ◽  
Dependent Pathway

ABSTRACT The biological response to endotoxin mediated through the Toll-like receptor 4 (TLR4)-MD-2 receptor complex is directly related to lipid A structure or configuration. Endotoxin structure may also influence activation of the MyD88-dependent and -independent signaling pathways of TLR4. To address this possibility, human macrophage-like cell lines (THP-1, U937, and MM6) or murine macrophage RAW 264.7 cells were stimulated with picomolar concentrations of highly purified endotoxins. Harvested supernatants from previously stimulated cells were also used to stimulate RAW 264.7 or 23ScCr (TLR4-deficient) macrophages (i.e., indirect induction). Neisseria meningitidis lipooligosaccharide (LOS) was a potent direct inducer of the MyD88-dependent pathway molecules tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 3α (MIP-3α), and the MyD88-independent molecules beta interferon (IFN-β), nitric oxide, and IFN-γ-inducible protein 10 (IP-10). Escherichia coli 55:B5 and Vibrio cholerae lipopolysaccharides (LPSs) at the same pmole/ml lipid A concentrations induced comparable levels of TNF-α, IL-1β, and MIP-3α, but significantly less IFN-β, nitric oxide, and IP-10. In contrast, LPS from Salmonella enterica serovars Minnesota and Typhimurium induced amounts of IFN-β, nitric oxide, and IP-10 similar to meningococcal LOS but much less TNF-α and MIP-3α in time course and dose-response experiments. No MyD88-dependent or -independent response to endotoxin was seen in TLR4-deficient cell lines (C3H/HeJ and 23ScCr) and response was restored in TLR4-MD-2-transfected human embryonic kidney 293 cells. Blocking the MyD88-dependent pathway by DNMyD88 resulted in significant reduction of TNF-α release but did not influence nitric oxide release. IFN-β polyclonal antibody and IFN-α/β receptor 1 antibody significantly reduced nitric oxide release. N. meningitidis endotoxin was a potent agonist of both the MyD88-dependent and -independent signaling pathways of the TLR4 receptor complex of human macrophages. E. coli 55:B5 and Vibrio cholerae LPS, at the same picomolar lipid A concentrations, selectively induced the MyD88-dependent pathway, while Salmonella LPS activated the MyD88-independent pathway.

Anti-inflammatory assessment of 3-Acetylmyricadiol in LPS-Stimulated Raw 264.7 Macrophages

2021 ◽  
Vol 24 ◽  
Author(s):  
Gazanfar Ahmad ◽  
Reyaz Hassan ◽  
Neerupma Dhiman ◽  
Asif Ali
Keyword(s):  
Nitric Oxide ◽  
Cell Viability ◽  
Ethyl Acetate ◽  
Mtt Assay ◽  
Bark Extract ◽  
Maximum Effect ◽  
Potential Candidate ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Action

Background: Pentacyclic triterpenoids are a biologically active class of phytoconstituents with diverse pharmacological activity including anti-inflammatory action. Objective: In the current study, we isolated 3-Acetylmyricadiol, a pentacyclic triterpenoid, from the ethyl acetate bark-extract of Myrica esculenta and evaluated it for anti-inflammatory potential. Methods: The ethyl acetate bark-extract of the M. esculenta was subjected to column chromatography to isolate 3-Acetylmyricadiol. MTT assay was performed to check cell viability. The production of proinflammatory mediators like Nitric oxide, IL-6, TNF-α was observed after administration of 5, 10, 20 μM of 3-Acetylmyricadiol in LPS-activated Raw 246.7 macrophages by the reported methods. Results: MTT assay indicated more than 90% cell viability up to 20 μM of 3-Acetylmyricadiol. The administration of 3-Acetylmyricadiol inhibited the production of Nitric oxide, IL-6, TNF-α in a dose-dependent manner significantly in comparison to LPS treated cells. The maximum effect was observed at 20 μM of 3-Acetylmyricadiol which resulted in 52.37, 63.10, 55.37 % inhibition of Nitric oxide, IL-6, TNF-α respectively. Conclusion: Our study demonstrated the anti-inflammatory action of 3-Acetylmyricadiol and can serve as a potential candidate in the development of the clinically efficient anti-inflammatory molecule.

scholarly journals Nitric oxide interacts with cholinoceptors to modulate insulin secretion by pancreatic β cells

2020 ◽  
Vol 472 (10) ◽  
pp. 1469-1480
Author(s):  
Bashair M. Mussa ◽  
Ankita Srivastava ◽  
Abdul Khader Mohammed ◽  
Anthony J. M. Verberne
Keyword(s):  
Nitric Oxide ◽  
Insulin Secretion ◽  
Cell Viability ◽  
Combined Treatment ◽  
No Production ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Tnf Α ◽  
Ifn Γ

Abstract Dysfunction of the pancreatic β cells leads to several chronic disorders including diabetes mellitus. Several mediators and mechanisms are known to be involved in the regulation of β cell secretory function. In this study, we propose that cytokine-induced nitric oxide (NO) production interacts with cholinergic mechanisms to modulate insulin secretion from pancreatic β cells. Using a rat insulinoma cell line INS-1, we demonstrated that β cell viability decreases significantly in the presence of SNAP (NO donor) in a concentration- and time-dependent manner. Cell viability was also found to be decreased in the presence of a combined treatment of SNAP with SMN (muscarinic receptor antagonist). We then investigated the impact of these findings on insulin secretion and found a significant reduction in glucose uptake by INS-1 cells in the presence of SNAP and SMN as compared with control. Nitric oxide synthase 3 gene expression was found to be significantly reduced in response to combined treatment with SNAP and SMN suggesting an interaction between the cholinergic and nitrergic systems. The analysis of gene and protein expression further pin-pointed the involvement of M3 muscarinic receptors in the cholinergic pathway. Upon treatment with cytokines, reduced cell viability was observed in the presence of TNF-α and IFN-γ. A significant reduction in insulin secretion was also noted after treatment with TNF-α and IFN-γ and IL1-β. The findings of the present study have shown for the first time that the inhibition of the excitatory effects of cholinergic pathways on glucose-induced insulin secretion may cause β cell injury and dysfunction of insulin secretion in response to cytokine-induced NO production.

scholarly journals Anti-Migraine Effect of the Herbal Combination of Chuanxiong Rhizoma and Cyperi Rhizoma and UPLC-MS/MS Method for the Simultaneous Quantification of the Active Constituents in Rat Serum and Cerebral Cortex

Molecules ◽  
2019 ◽  
Vol 24 (12) ◽  
pp. 2230 ◽  
Author(s):  
Sha Wu ◽  
Li Guo ◽  
Feng Qiu ◽  
Muxin Gong
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Cortex ◽  
Cerebral Blood Flow ◽  
Mrna Expression ◽  
Enzyme Linked Immunosorbent Assay ◽  
Therapeutic Effects ◽  
Rat Serum ◽  
Active Constituents ◽  
Simultaneous Quantification

Chuanxiong Rhizoma and Cyperi Rhizoma (CRCR), an ancient and classic formula comprised of Chuanxiong Rhizoma and Cyperi Rhizoma in a weight ratio of 1:2, has long been used for curing migraine. This study aimed to explore their anti-migraine effect and active constituents. A nitroglycerin (NTG)-induced migraine model in rats was established to evaluate pharmacological effects. Cerebral blood flow was detected by a laser Doppler perfusion monitor. The levels of endothelin-1 (ET-1), γ-aminobutyric acid (GABA), nitric oxide synthase (NOS), nitric oxide (NO), 5-hydroxytryptamine (5-HT), 5-hydoxyindoleacetic acid (5-HIAA), calcitonin gene-related peptide (CGRP) and β-endorphin (β-EP) were quantified with enzyme-linked immunosorbent assay. CGRP and c-Fos mRNA expression were quantified with quantitative real-time polymerase chain reaction. A UPLC-MS/MS method was developed and validated for the simultaneous quantification of active constituents in rat serum and cerebral cortex. CRCR significantly increased cerebral blood flow, decreased the levels of ET-1, GABA and NOS, and increased the levels of 5-HT, 5-HIAA and β-EP in NTG-induced migraine rats. CGRP levels and CGRP mRNA expression, as well as c-Fos mRNA expression in the brainstem were markedly down-regulated with the treatment of CRCR. After oral administration of CRCR, ferulic acid (FA), senkyunolide A (SA), 3-n-butylphthalide (NBP), Z-ligustilide (LIG), Z-3-butylidenephthalide (BDPH), cyperotundone (CYT), nookatone (NKT) and α-cyperone (CYP) were qualified in rat serum and cerebral cortex. The above results suggested that CRCR showed powerfully therapeutic effects on migraine via increasing the cerebral blood flow, decreasing the expression of CGRP and c-Fos mRNA, and regulating the releasing of ET-1, GABA, NOS, 5-HT, 5-HIAA, CGRP and β-EP in the serum and brainstem, consequently relieving neurogenic inflammation. The active constituents in CRCR for treating migraine were FA, SA, NBP, LIG, BDPH, CYT, NKT and CYP. These findings contributed for the further use of CRCR as a combinational and complementary phytomedicine for migraine treatment.

scholarly journals Effect of nitric oxide release from NOR-3 on urea synthesis, viability and oxygen consumption of rat hepatocyte cultures

2007 ◽  
pp. 427-432
Author(s):  
R Chimenti ◽  
G Martino ◽  
S Mazzulla ◽  
S Sesti
Keyword(s):  
Nitric Oxide ◽  
Oxygen Consumption ◽  
Cell Viability ◽  
Urea Synthesis ◽  
Rat Hepatocyte ◽  
Trypan Blue Exclusion ◽  
No Donor ◽  
Nitric Oxide Release ◽  
Hepatocyte Cultures ◽  
Trypan Blue Exclusion Test

As nitric oxide is considered a mediator of liver oxidative metabolism during sepsis, we studied the effects of exogenous nitric oxide, produced by NO-donor, (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (NOR-3), on cell viability, urea biosynthesis and oxygen consumption in rat hepatocyte cultures. Nitric oxide release from NOR-3 was studied using 4,5-diaminofluorescein diacetate. Urea levels were measured by the spectrophotometric method. Cell viability was determined by the MTT test and trypan blue exclusion test, whereas oxygen consumption was measured by a polarographic technique. After 2 h treatment, NOR-3 induced an increase in the levels of nitric oxide. After 2 h of treatment and 24 h after the end of the treatment with NOR-3, both cell viability and urea synthesis were significantly reduced in comparison to the controls for NOR-3 concentrations equal to or greater than 50 microM. A reduction in oxygen consumption was observed in hepatocytes after 40 min treatment with 100 microM NOR-3, even if the cell viability was unchanged. Reduction of oxygen consumption is an early indicator of the metabolic alterations in hepatocytes exposed to nitric oxide. These findings suggest that nitric oxide accumulation acts on hepatocyte cultures inducing cell death and reduction of urea synthesis after 2 hours.

scholarly journals Novel non-specific lipid-Transfer Protein (TdLTP4) isolated from Durum wheat: Antimicrobial activities to control pathogen and spoilage bacteria and Anti-Inflammatory properties in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages

2020 ◽  
Author(s):  
Anis Ben Hsouna ◽  
Rania Ben Saad ◽  
Wissal Dhifi ◽  
Marwa Khaled ◽  
Wissem Mnif ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Fusion Protein ◽  
Supernatant Fraction ◽  
Enzyme Linked Immunosorbent Assay ◽  
Raw 264.7 ◽  
Lipid Transfer ◽  
Raw 264.7 Macrophages ◽  
Tnf Α ◽  
Spoilage Bacteria ◽  
Anti Inflammatory

Abstract Background: Lipid transfer proteins (LTP) are members of the family of pathogenesis-related proteins (PR-14) that play a key role in plant defense mechanisms.Methods: In this study, a novel gene TdLTP4 encoding an antifungal protein from wheat (cv. Om Rabiaa) was subcloned, overexpressed in Escherichia coli BL-21 (DE3) and enriched using ammonium sulfate fractionation. The TdLTP4 fusion protein was then tested against a panel of pathogens, food-borne and spoilage bacteria and fungi in order to evaluate the antimicrobial properties. Our protein was applied to 0.5 µg/mL LPS-induced RAW 264.7 macrophages in vitro at different concentrations (5, 10, 20, 50 and 100 µg/ml). Levels of nitric oxide (NO), pro-inflammatory cytokines interleukin (IL)-1β (IL-1 β), interleukin (IL)-6 (IL-6), tumor necrosis factor (TNF-α) and anti-inflammatory cytokine IL-10 in the supernatant fraction were measured using enzyme-linked immunosorbent assay (ELISA). Expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were detected via Western blot. Results: The inhibition zones and minimal inhibitory concentration (MIC) values of bacterial strains were in the range of 14-26 mm and 62.5-250 µg/mL, respectively. Moreover, a remarkable activity against several fungal strains was revealed. TdLTP4 (5–100 µg/mL) decreased the production of NO (IC50= 4.32 µg/mL), IL-6 (IC50= 11.52 µg/mL), IL-1β (IC50= 7.87 µg/mL) and TNF-α (IC50 =8.66 µg/mL) by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Our protein could modulate the macrophages inflammatory mode by causing reduction in iNOS and COX2.Conclusion: According to these findings, LTP fusion protein could be used as natural anti-inflammatory and antimicrobial agent in food preservation and human health.

scholarly journals Saussurea lappa Clarke extract exhibits potent antioxidant effect and attenuates neuroinflammatory responses in lipopolysaccharide-stimulated microglial cells

2020 ◽  
Vol 19 (9) ◽  
pp. 1911-1917
Author(s):  
Sung-Gyu Lee ◽  
Hyun Kang
Keyword(s):  
Nitric Oxide ◽  
Radical Scavenging Activity ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Enzyme Linked Immunosorbent Assay ◽  
No Production ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Saussurea Lappa ◽  
Tnf Α

Purpose: To investigate the antioxidant and anti-neuroinflammatory potential of Saussurea lappa Clarke (SLC-EA) extract in LPS-stimulated BV-2 microglial cells.Methods: Cell viability was measured by using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay while antioxidant activity was evaluated by using the DPPH (1,1-diphenyl-2-picrylhydrazyl) radical scavenging activity. Lipopolysaccharide (LPS) was used to stimulate BV-2 microglia. Griess assay was employed to assess nitric oxide (NO) production. iNOS (inducible NO synthase) expression and TNF-α (tumor necrosis factor-alpha) cytokine production were measured by ELISA (enzyme-linked immunosorbent assay) and immuno blot analysis, respectively.Results: Pretreatment of 100 mg/ml of SLC-EA (p < 0.001) was inhibited Nitric Oxide (NO) by 1 ug/ml of LPS-treated murine BV-2 cells. The expression of iNOS and TNF-α were reduced by SLC-EA concentration dependent manner (p < 0.001 at 100 mg/ml). SLC-EA were scavenged 1, 1-diphenyl-2-picrylhydrazyl (DPPH) radicals in a dose-dependent manner with an IC50 value of approximately 51.4 μg/ml.Conclusion: The results indicate that SLC-EA extract exhibits strong antioxidant properties and inhibits excessive pro-inflammatory cytokine due probably to the antioxidant phenolic compounds present in SLC-EA extract. Further work in exploring the in-depth mechanisms of SLC-EA extract in regulating inflammatory signaling pathways in treating neuroinflammatory diseases is necessary. Keywords: Saussurea lappa, Antioxidant, Neuroinflammation, Microglia, TNF-α, iNOS

scholarly journals MiR-146b-3p protects against AR42J cell injury in cerulein-induced acute pancreatitis model through targeting Anxa2

2021 ◽  
Vol 16 (1) ◽  
pp. 255-265
Author(s):  
Kunpeng Zhang ◽  
Xiaoyu Zhang
Keyword(s):  
Acute Pancreatitis ◽  
Cell Viability ◽  
Cell Injury ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Qrt Pcr ◽  
Ar42j Cells ◽  
Tnf Α ◽  
Ar42j Cell

Abstract Background Acute pancreatitis (AP) is a common inflammatory disorder. MicroRNAs play crucial roles in the pathogenesis of AP. In this article, we explored the detailed role and molecular mechanisms of miR-146b-3p in AP progression. Methods The rat AR42J cells were treated with cerulein to establish the AP model in vitro. The miR-146b-3p and Annexin A2 (Anxa2) mRNA levels were assessed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Cell viability and apoptosis were tested using the Cell Counting Kit-8 (CCK-8) and flow cytometry assays, respectively. Caspase-3 activity and the production of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were measured by enzyme-linked immunosorbent assay and qRT-PCR. Targeted interaction between miR-146b-3p and Anxa2 was verified by the dual-luciferase reporter and RNA immunoprecipitation assays. Western blot analysis was performed to detect the expression of Anxa2 protein. Results Our data revealed that miR-146b-3p was significantly downregulated in AP samples. The enforced expression of miR-146b-3p alleviated cerulein-induced injury in AR42J cells, as evidenced by the promotion in cell viability and the repression in cell apoptosis, as well as the reduction in IL-1β, IL-6, and TNF-α production. Anxa2 was directly targeted and inhibited by miR-146b-3p. Moreover, the alleviative effect of miR-146b-3p overexpression on cerulein-induced AR42J cell injury was mediated by Anxa2. Conclusions The current work had led to the identification of miR-146b-3p overexpression that protected against cerulein-induced injury in AR42J cells at least in part by targeting Anxa2, revealing a promising target for AP diagnosis and treatment.

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