Αρχειοθήκη ιστολογίου

Δευτέρα 15 Μαρτίου 2021

Interleukin-1β weakens paclitaxel sensitivity through regulating autophagy in the non-small cell lung cancer cell line A549

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Exp Ther Med. 2021 Apr;21(4):293. doi: 10.3892/etm.2021.9724. Epub 2021 Jan 27.

ABSTRACT

Non-small cell lung cancer (NSCLC) poses a threat to human health and paclitaxel chemotherapy has been approved for the treatment of this type of cancer. However, resistance to treatment severely compromises the survival rate and prognosis of patients with NSCLC. The aim of the present study was to investigate the role of IL-1β in paclitaxel sensitivity of NSCLC cells and elucidate the underlying mechanism. The expression of IL-1β was found to be upregulated in NSCLC tissues and cells compared with healthy adjacent tissues and a normal epithelial cell line, respectively, as detected by reverse transcription-quantitative PCR and western blot analyses. Subsequently, Cell Counting Kit-8 assay and flow cytometry revealed that IL-1β weakened the sensitivity of A549 cells to paclitaxel. It was subsequently demonstrated that IL-1β induced A549 cell au tophagy, while tunicamycin-induced autophagy increased the IL-1β expression level and weakened paclitaxel sensitivity. Thus, the results revealed that IL-1β reduced the sensitivity to paclitaxel in A549 cells by promoting autophagy and suggested that IL-1β may be of value for improving the therapeutic efficacy of paclitaxel chemotherapy in NSCLC.

PMID:33717236 | PMC:PMC7885084 | DOI:10.3892/etm.2021.9724

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Novel immunological and genetic factors associated with vitiligo: A review

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Exp Ther Med. 2021 Apr;21(4):312. doi: 10.3892/etm.2021.9743. Epub 2021 Feb 1.

ABSTRACT

Vitiligo is a skin disorder characterized by depigmentation of the skin due to a lack of melanin. This condition affects men and woman of all ages and its incidence is not restricted by ethnicity or region. Vitiligo is a multifactorial disease, in which melanocytes, which serve important functions in skin pigmentation and immune processes, are impaired. There is sufficient evidence that immunological and genetic factors are primarily responsible for the destruction and dysfunction of melanocytes. Therefore, genetic DNA sequence variants that participate in skin homeostasis, pigmentation and immune response regulation, as well as altered expression patterns, may contribute to the risk of developing vitiligo. The current review presented an overview of the mechanism of pigmentation and of currently known factors involved in depigmentation, as well as the classification, epidemiology, associated comorbidities, risk factors, immunopathogenesis and several genetic and molecular changes associated with vitiligo.

PMID:33717255 | PMC:PMC7885061 | DOI:10.3892/etm.2021.9743

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Hesperetin attenuates silica-induced lung injury by reducing oxidative damage and inflammatory response

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Exp Ther Med. 2021 Apr;21(4):297. doi: 10.3892/etm.2021.9728. Epub 2021 Jan 28.

ABSTRACT

Oxidative stress and the inflammatory response are two important mechanisms of silica-induced lung injury. Hesperetin (HSP) is a natural flavonoid compound that is found in citrus fruits and has been indicated to exhibit strong antioxidant and anti-inflammatory properties. The current study evaluated the protective effect of HSP on lung injury in rats exposed to silica. The results indicated that the degree of alveolitis and pulmonary fibrosis in the HSP-treated group was significantly decreased compared with the silica model group. The content of hydroxyproline (HYP) was also revealed to decrease overall in the HSP treated group compared with the silica model group, indicating that the degree of pulmonary fibrosis was decreased compared with the silica model group. The present study also demonstrated that HSP reduced oxidation levels of malondiald ehyde (MDA) and increased the activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX). Total antioxidant capacity (T-AOC) was also increased following HSP treatment, indicating that HSP can alleviate oxidative stress in the lung tissue of silica-exposed rats. In addition, HSP was revealed to inhibit the synthesis and secretion of fibrogenic factor TGF-β1, reduce the production of pro-inflammatory cytokines IL-1β, IL-4, TNF-α and increase the levels of anti-inflammatory factors IFN-γ and IL-10. The current study demonstrated that HSP can effectively attenuate silica-induced lung injury by reducing oxidative damage and the inflammatory response.

PMID:3371724 0 | PMC:PMC7885076 | DOI:10.3892/etm.2021.9728

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TRIB3 promotes oral squamous cell carcinoma cell proliferation by activating the AKT signaling pathway

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Exp Ther Med. 2021 Apr;21(4):313. doi: 10.3892/etm.2021.9744. Epub 2021 Feb 1.

ABSTRACT

Tribbles pseudokinase 3 (TRIB3), a member of the tribbles-related family, has biological roles such as by acting as an oncogene or tumor suppressor gene, in various types of cancer, including colorectal cancer, breast cancer, lung cancer and renal cell carcinoma. However, the role of TRIB3 in oral squamous cell carcinoma (OSCC) is remains unclear. The current was aimed to determine the biological function of TRIB3 in OSCC progression. TRIB3 expression was examined in OSCC surgical specimens using reverse transcription-quantitative PCR and the role of TRIB3 in the proliferation capacities of OSCC cell lines was examined using crystal violet and MTT assays in vitro and tumorigenicity assays in vivo. The underlying mechanism by which TRIB3 exerts its function was investigated using western blotting. The results demonstrated that the mRNA and protein expression levels of TRIB3 were higher in human OSCC tissues compared with normal tissues. The role of TRIB3 in cell proliferation was also determined. TRIB3 overexpression significantly promoted OSCC cell proliferation, whereas TRIB3 knockdown inhibited OSCC cell proliferation compared with control cells. TRIB3 knockdown also suppressed tumor growth and decreased tumor volume in vivo compared with control cells. Moreover, the results suggested that TRIB3 overexpression increased the phosphorylation of protein kinase B (AKT) and mammalian target of rapamycin (mTOR), whereas TRIB3 knockdown decreased the phosphorylation of AKT and mTOR compared with control cells. To summarize, the present study indicated that TRIB3 promoted OSCC cell proliferation by activating the AKT signaling pathway; therefore, TRIB3 may serve as a potential target for the diagnosis and treatment of OSCC.

PMID:33717256 | PMC:PMC7885083 | DOI:10.3892/etm.2021.9744

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MicroRNA-432-5p inhibits cell migration and invasion by targeting CXCL5 in colorectal cancer

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Exp Ther Med. 2021 Apr;21(4):301. doi: 10.3892/etm.2021.9732. Epub 2021 Jan 29.

ABSTRACT

MicroRNAs (miRNAs) play an important role in the occurrence and development of colorectal cancer (CRC). Evidence shows that miR-432-5p expression is decreased in various tumors and cancer cell lines. miR-432-5p can inhibit tumor invasion and metastasis, but its role in colorectal cancer is unclear. The present study demonstrated that miR-432-5p expression was decreased in colorectal cancer tissue and cell lines, and is negatively associated with invasion classification, lymph node metastasis and Tumor-Node-Metastasis stage. Kaplan-Meier survival analysis showed that low miR-432-5p expression was associated with a poor survival rate in patients with CRC. In addition, SW480 and HT-29 cells transfected with miR-432-5p mimics had decreased migration and invasion abilities, whereas miR-432-5p inhibitors had the opposite effect. The expression of C-X-C m otif chemokine ligand 5 (CXCL5), a direct target of miR-432-5p, was negatively associated with miR-432-5p expression. When CXCL5 was introduced into miR-432-5p mimic-transfected SW480 and HT-29 cells, miR-432-5p-mediated inhibition of CRC migration and invasion was reversed. Thus, the present results suggest that miR-432-5p can inhibit the migration and invasion of CRC cells by targeting CXCL5.

PMID:33717244 | PMC:PMC7885074 | DOI:10.3892/etm.2021.9732

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Biological role of postoperative low level laser therapy in preventing hydroxyapatite orbital implantation exposure: A case report

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Exp Ther Med. 2021 Apr;21(4):314. doi: 10.3892/etm.2021.9745. Epub 2021 Feb 3.

ABSTRACT

Conjunctival sac stenosis is the contraction of the conjunctival sac as a result of trauma or disease. The aim of the present study was to observe the clinical effects of low-level laser therapy (LLLT) combined with hydroxyapatite (HA) orbital implantation as a treatment strategy for conjunctival sac stenosis. A total of 10 patients with conjunctival sac stenosis were treated with scleral graft transplantation in conjunction with HA implantation and postoperative LLLT. In addition, a rabbit model was used to investigate the biological mechanism underlying the effects of LLLT with the aim of preventing and treating orbital implantation exposure. The right eyeball was removed, orbital implantation performed and LLLT applied to experimental groups. 99mTc-Methyl diphosphonate scanning methods were performed at different timepoints to compare the average radioactivity count of the region of interest between surgical (right) and control (left) eyes (R/L). Histopathological examination was performed 8 weeks post-surgery, followed by analysis of fiber vascularization. Following LLLT, moderate conjunctival wounds were completely healed within 2 weeks and severe stenosis wounds healed within 3 weeks. Following prosthesis implantation in the rabbit model, a significantly elevated R/L ratio was observed after 4 weeks, whereas no significant difference was observed compared with the control group at 6 and 8 weeks postoperatively. Histopathological examination revealed that all implants were fibrotic. Overall, the present study demonstrated that LLLT promoted the survival of conjunctival grafts, stimulated conjunctival incision healing and promoted early vascularization of HA implants. Clinical trial registration no: ChiCTR-DDT-12002660 (www.chictr.org/cn/).

PMID:33717257 | PMC:PMC7885064 | DOI:10.3892/etm.2021.9745

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Interleukin-6 released by oral lichen planus myofibroblasts promotes angiogenesis

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Exp Ther Med. 2021 Apr;21(4):291. doi: 10.3892/etm.2021.9722. Epub 2021 Jan 27.

ABSTRACT

Oral lichen planus (OLP), defined as a potential for malignant transformation, is a chronic inflammatory disease in which abnormal angiogenesis serves a role in the malignant changes of the disease. OLP-associated fibroblasts (OLP-MFs), derived from the stroma of OLP tissues, are characterized by the presence of myofibroblasts and contribute to the secretion of pro-inflammatory cytokines, which may be involved in the molecular pathogenesis of OLP. However, the associated mechanisms of angiogenesis in OLP remain unknown. The present study aimed to verify the expression of intercellular adhesion molecular 1, vascular cell adhesion molecule 1, VEGF and CD34 in OLP, and to investigate whether IL-6 secreted by OLP-MFs promoted OLP angiogenesis and the effect of its corresponding antibody inhibition. The results of the experiments demonstrated that infla mmation was present and OLP upregulated the secretion of IL-6 by OLP stromal fibroblasts, thereby enhancing OLP angiogenesis. Anti-IL-6 receptor antibody inhibited OLP-stroma IL-6 signaling and suppressed OLP angiogenesis. The antibody inhibited the inflammatory response by inhibiting the secretion of inflammatory factors, including IL-6, to suppress angiogenesis and reduce disease progression, thus indicating that this could be a potential target to develop a treatment for OLP.

PMID:33717234 | PMC:PMC7885057 | DOI:10.3892/etm.2021.9722

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Chronic atrophic gastritis and intestinal metaplasia induced by high-salt and N-methyl-N'-nitro-N-nitrosoguanidine intake in rats

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Exp Ther Med. 2021 Apr;21(4):315. doi: 10.3892/etm.2021.9746. Epub 2021 Feb 3.

ABSTRACT

The aim of the present study was to induce chronic atrophic gastritis (CAG) with intestinal metaplasia (IM) in rats by administering saturated salt and methyl-N'-nitro-N-nitrosoguanidine (MNNG) via oral gavage. Changes in gastric mucosal blood microcirculation and activation of the cyclo-oxygenase-2 (COX-2)/hypoxia inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway during CAG and IM development were investigated. After administering saturated salt and MNNG for 25 weeks, mild atrophy was detected in the stomach of model rats using hematoxylin and eosin staining. CAG with IM was successfully induced in the gastric mucosa of the model rats after 35 weeks. Gastric mucosal blood flow was decreased in comparison with controls as early as 15 weeks after treatment to induce CAG and the mRNA expression levels of COX-2, HIF-1α, vascular endothelial growth factor receptor (VEGFR)1 and VEGFR2 were increased in comparison with untreated rats as early as 25 weeks after treatment. HIF-1α, COX-2 and VEGFR2 expression levels were increased as early as 25 weeks after CAG induction treatment when compared to controls and HIF-1α, COX-2, VEGFR1 and VEGFR2 expression levels were significantly increased after 35 weeks. These findings indicated that administering saturated salt and MNNG by gavage for 35 weeks successfully induced CAG and IM in rats. Furthermore, the microcirculation was disturbed before activation of the COX-2/HIF-1α/VEGF signaling pathway.

PMID:33717258 | PMC:PMC7885066 | DOI:10.3892/etm.2021.9746

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Comparison of the application value of two commonly used minimally invasive spinal surgery in the treatment of lumbar disc herniation

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Exp Ther Med. 2021 Apr;21(4):299. doi: 10.3892/etm.2021.9730. Epub 2021 Jan 28.

ABSTRACT

The aim of the study was to compare the application value of percutaneous transforaminal endoscopic discectomy (PTED) and microendoscopic discectomy (MED) in the treatment of lumbar disc herniation (LDH). From January 2017 to July 2018, 108 LDH patients undergoing surgical treatment in our hospital were collected and divided into PTED group (treated with PTED, n=50) and MED group (treated with MED, n=58). The operation parameter index level, complications, recurrence and pain score (VAS), Oswestry disability index (ODI) and Japanese Orthopaedic Association Scale (JOA) were compared between the two groups. VAS, ODI and JOA scores of the two groups were significantly decreased after operation (P<0.05), but there was no significant difference between the two groups (P>0.05). Complications and recurrence of the two groups were similar (P>0.05) . MED was superior to PTED in the number of intraoperative fluoroscopy and operation time, while PTED was superior to MED in intraoperative blood loss, incision length, length of hospital stay and bed rest time (P<0.05). Both PTED and MED can effectively treat LDH. Referring to clinical data, PTED may be the first choice for LDH treatment.

PMID:33717242 | PMC:PMC7885071 | DOI:10.3892/etm.2021.9730

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Comparison of the application value of two commonly used minimally invasive spinal surgery in the treatment of lumbar disc herniation

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Exp Ther Med. 2021 Apr;21(4):299. doi: 10.3892/etm.2021.9730. Epub 2021 Jan 28.

ABSTRACT

The aim of the study was to compare the application value of percutaneous transforaminal endoscopic discectomy (PTED) and microendoscopic discectomy (MED) in the treatment of lumbar disc herniation (LDH). From January 2017 to July 2018, 108 LDH patients undergoing surgical treatment in our hospital were collected and divided into PTED group (treated with PTED, n=50) and MED group (treated with MED, n=58). The operation parameter index level, complications, recurrence and pain score (VAS), Oswestry disability index (ODI) and Japanese Orthopaedic Association Scale (JOA) were compared between the two groups. VAS, ODI and JOA scores of the two groups were significantly decreased after operation (P<0.05), but there was no significant difference between the two groups (P>0.05). Complications and recurrence of the two groups were similar (P>0.05) . MED was superior to PTED in the number of intraoperative fluoroscopy and operation time, while PTED was superior to MED in intraoperative blood loss, incision length, length of hospital stay and bed rest time (P<0.05). Both PTED and MED can effectively treat LDH. Referring to clinical data, PTED may be the first choice for LDH treatment.

PMID:33717242 | PMC:PMC7885071 | DOI:10.3892/etm.2021.9730

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Effect and related mechanism of Yinchenhao decoction on mice with lithogenic diet-induced cholelithiasis

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Exp Ther Med. 2021 Apr;21(4):316. doi: 10.3892/etm.2021.9747. Epub 2021 Feb 3.

ABSTRACT

The aim of the present study was to investigate the effects and the underlying mechanisms of Yinchenhao Decoction (YCHD), a traditional Chinese medicine formulation, on C57BL/6 mice with lithogenic diet (LD)-induced cholelithiasis. The condition of cholelithiasis was evaluated using a six-level criteria. Levels of alanine aminotransferase (ALT), alkaline phosphatase (ALP), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) in the serum and liver tissue were measured using enzyme colorimetry. Concentrations of TC, phospholipids (PL) and total bile acids (TBA) in the bile were measured to calculate the cholesterol saturation index. Liver histopathology was microscopically observed and mRNA expression levels of ABCG5, ABCG8, SRBI, ABCB4, ABCB11 and NPC1L1 involved in cholesterol metabolism were measured using reverse transcription-quan titative PCR. The results showed that feeding mice the LD induced cholelithiasis, along with abnormal serum biochemical indices and imbalances in biliary cholesterol homeostasis. Increased ALT and ALP levels in the serum and ALT, ALP, TC and LDL-C levels in the serum and liver indicated the existence of hepatocyte injury, which were consistent with the pathological changes. YCHD treatment ameliorated the serum and hepatic biochemical abnormalities and adjusted the biliary imbalance. In addition, elevated expression of ATP-binding cassette subfamily G member 5/8, scavenger receptor class B type I and Niemann-Pick C1 Like 1 in the liver and small intestine were observed at the onset of cholelithiasis but were reversed by YCHD. Taken together, results from the present study suggest that YCHD ameliorated LD-induced cholelithiasis mice, which may be caused by improvements in biliary cholesterol supersaturation and regulation of cholesterol metabolism.

PMID:33717259 | PMC:PMC7885065 | DOI:10.3892/etm.2021.9747

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