Berrybager7849

The plant extract piperine is used as a traditional Chinese medicine due to its anti‑inflammatory effects and efficacy against numerous types of cancer. The aim of the present study was to investigate the antitumor mechanism of piperine in human osteosarcoma U2OS and 143B cell lines. The effects of piperine on cell apoptosis and invasion of human osteosarcoma cells were assessed using flow cytometry and Transwell assays. Moreover, western blotting was used to measure the effects of piperine on the protein expression levels of the metastasis markers matrix metalloproteinase‑2 (MMP‑2) and vascular endothelial growth factor (VEGF). In addition, the involvement of the Wnt/β‑catenin signaling pathway in modulating the effects of piperine was examined via western blot analysis. The results of MTT and Transwell invasion assays indicated that piperine treatment dose‑dependently reduced U2OS and 143B cell viability and invasion. Furthermore, a significant reduction was identified in MMP‑2, VEGF, glycogen synthase kinase‑3β and β‑catenin protein expression levels, as well as the expression levels of their target proteins cyclooxygenase‑2, cyclin D1 and c‑myc, in U2OS cells after piperine treatment. In addition, similar results were observed in 143B cells. Therefore, the present study demonstrated the efficacy of piperine in osteosarcoma, and identified that the Wnt/β‑catenin signaling pathway may modulate the antitumor effects of piperine on human U2OS and 143B cells.Acute lung injury (ALI) is characterized by tissue damage and inflammatory cytokine secretion; however, the therapeutic options available to treat ALI remain limited. Necrostatin‑1 (Nec‑1) has the ability to attenuate cell necroptosis in various inflammatory diseases. The present study evaluated the protective effects of Nec‑1 on a mouse model of lipopolysaccharide‑induced ALI. Histological alterations in the lungs were evaluated through hematoxylin and eosin staining, and the expression levels of cytokines in the bronchoalveolar lavage fluid and lung tissues were determined by ELISA. In addition, accumulated production of reactive oxygen species was determined by staining with DCFH‑DA probes, western blotting and immunofluorescence. The results revealed that treatment with the necroptosis inhibitor, Nec‑1, exerted significant protective effects on ALI‑induced inflammation and necroptosis. The key proteins involved in necroptosis were markedly reduced, including receptor‑interacting serine/threonine‑protein kinase (RIP)1 and RIP3. Notably, antioxidant proteins were upregulated by Nec‑1, which may attenuate oxidative stress. Furthermore, treatment with Nec‑1 markedly suppressed necroptosis in the pulmonary alveoli RLE‑6TN cell line. Taken together, these data revealed a novel association between ALI and necroptosis, and suggested that necroptosis inhibitors may be used as effective anti‑inflammatory drugs to treat ALI.Subsequently to the publication of the above paper, the authors have realized that Fig. 6E and F contained errors. Essentially, some of the data shown in Fig. 6E were incorrect, and consequently, the quantification of the data illustrated in Fig. 6F were likewise incorrect. The corrected version of Fig. 6, showing the correct data for these figure parts, is shown opposite. Note that these errors in the data selection for this figure did not seriously affect the overall conclusions reported in the study. The authors are grateful to the Editor for allowing them the opportunity to publish this Corrigendum, and wish to apologize to the readership of the Journal for any inconvenience caused. [the original article was published in Molecular Medicine Reports 21 320‑328, 2020; DOI 10.3892/mmr.2019.10839].Excessive adipose tissue accumulation is an increasing health problem worldwide. The present study aimed to determine differentially expressed genes (DEGs) that are associated with the excessive accumulation of adipose tissues by PCR arrays in an excess dietary intake animal model. For this purpose, male Sprague Dawley rats were randomly assigned to 2 groups Control (given an ordinary diet) and experimental (given twice the amount of the ordinary diet). After 2 months of feeding, the abdominal cavities of the rats from each group were opened, then subcutaneous and visceral adipose tissues were removed. The adipose tissues collected were then used for total RNA extraction and then reverse transcribed to cDNA, which was then used as a template to identify the DEGs of 84 transcripts for rat obesity by RT2 Profiler PCR Arrays. The results showed significant downregulation of bombesin‑like receptor 3 (BRS3) and uncoupling protein 1 (UCP1) in visceral adipose tissues of experimental rats compared with those of the control rats, and differential gene expression analysis showed an association with fat cell differentiation and regulation of triglyceride sequestration, as well as fatty acid binding. The gene expression patterns observed in the present study, which may be associated with peroxisome proliferator‑activated receptor‑γ (PPARG) on excessive visceral adipose tissue accumulation, may be useful in identifying a group of surrogate biomarkers for the early diet‑induced accumulation of visceral adipose tissue detection in humans. The biomarkers can also be the specific targets for drug development to reduce excessive visceral adipose tissue accumulation in the body and its associated diseases.The present study aimed to investigate whether the cytoskeleton, the Piezo1 ion channel and the transient receptor potential cation channel subfamily V member 4 (TRPV4) ion channel are equally functional in the mechanotransduction of periodontal ligament cells (PDLCs) and to reveal the interplay of these mechanically sensitive ion channels (MSCs). Human PDLCs (hPDLCs) were pretreated with cytochalasin D (the inhibitor of actin polymerization), GsMTx4 (the antagonist of Piezo1) and GSK205 (the antagonist of TRPV4), and then subjected to periodic mechanical loading. The expression levels of macrophage colony stimulating factor (M‑CSF), receptor activator of NF‑κB ligand (RANKL) and cyclooxygenase‑2 (COX2) in hPDLCs were detected via western blotting. Osteoblast mineralization induction capacity of the hPDLCs was also studied and the mitogen‑activated protein kinase (MAPK) expression profile was determined via protein microarray. The expression of Piezo1 and TRPV4 in the PDLCs was significantly increased at 8 h after loading. read more These differences in expression were accompanied by increased expression of M‑CSF, RANKL and COX2. Compared with the control group, key PDLC biomarkers were suppressed after mechanical loading following treatment with the inhibitors of Piezo1 (GsMTx4) and TRPV4 (GSK205). The phosphorylated‑MAPK protein array showed differential biomarker profiles among all groups. The present study suggested that both MSCs and the cytoskeleton participated as mechanical sensors, and did so independently in hPDLC mechanotransduction. Furthermore, the Piezo1 ion channel may transmit mechanical signals via the ERK signaling pathway; however, the TRPV4 channel may function via alternative signaling pathways.Ischemic stroke is one of the leading causes of mortality and disability worldwide. However, there is a current lack of effective therapies available. As the resident macrophages of the brain, microglia can monitor the microenvironment and initiate immune responses. In response to various brain injuries, such as ischemic stroke, microglia are activated and polarized into the proinflammatory M1 phenotype or the anti‑inflammatory M2 phenotype. The immunomodulatory molecules, such as cytokines and chemokines, generated by these microglia are closely associated with secondary brain damage or repair, respectively, following ischemic stroke. It has been shown that M1 microglia promote secondary brain damage, whilst M2 microglia facilitate recovery following stroke. In addition, autophagy is also reportedly involved in the pathology of ischemic stroke through regulating the activation and function of microglia. Therefore, this review aimed to provide a comprehensive overview of microglia activation, their functions and changes, and the modulators of these processes, including transcription factors, membrane receptors, ion channel proteins and genes, in ischemic stroke. The effects of autophagy on microglia polarization in ischemic stroke were also reviewed. Finally, future research areas of ischemic stroke and the implications of the current knowledge for the development of novel therapeutics for ischemic stroke were identified.Diabetes mellitus (DM) contributes to intervertebral disc degeneration (IDD). The long non‑coding RNA MALAT1 has been revealed to play an important role in diabetes‑associated complications. However, the specific role of MALAT1 in diabetes‑associated IDD has not been determined. The aim of the present study was to evaluate the roles of MALAT1 in the apoptosis of cartilage endplate (CEP) cells induced by high glucose and to explore the mechanisms underlying this effect. Rat CEP cells were cultured in high‑glucose medium (25 mM glucose) for 24 or 72 h. Cells cultured in medium containing 5 mM glucose were used as a control. Flow cytometry was used to detect the degree of apoptosis. Reverse transcription‑quantitative PCR was used to measure the expression of MALAT1 mRNA. In addition, CEP cells were treated with different conditions (high glucose, high glucose + MALAT1 negative control, high glucose + MALAT1 RNAi, normal control) for 72 h. Flow cytometry was subsequently used to detect apoptosis and western blotting was used to measure the expression levels of total and phosphorylated p38. The results revealed that high glucose concentration promoted apoptosis and enhanced expression of MALAT1 in CEP cells. Furthermore, MALAT1 knockout decreased the expression levels of total and phosphorylated p38 and reduced the apoptosis of rat CEP cells. The results obtained in the present study indicated that MALAT1 may serve as an important therapeutic target for curing or delaying IDD in patients with diabetes.Vascular remodeling plays an important role in the pathogenesis of diabetic cardiovascular complications. Previous published research has indicated that microRNA‑24 (miR‑24) is involved in diabetic vascular remodeling, but the underlying molecular mechanisms have yet to be fully elucidated. The aim of the present study was to investigate whether adenovirus‑mediated miR‑24 overexpression can suppress the NOD‑like receptor family pyrin domain‑containing 3 (NLRP3)‑related inflammatory signaling pathway and attenuate diabetic vascular remodeling. The carotid arteries of diabetic rats were harvested and prepared for analysis. Reverse transcription‑quantitative PCR and western blotting assays were used to detect the expressions of related mRNAs and proteins. Morphological examinations, including hematoxylin and eosin, immunohistochemical and Masson's trichrome staining, were also performed. The results of the present study demonstrated that miR‑24 upregulation suppressed neointimal hyperplasia and accelerated reendothelialization in the injured arteries, lowered the expression of NLRP3, apoptosis‑associated speck‑like protein, caspase‑1, proliferating cell nuclear antigen, CD45, interleukin (IL)‑1β, IL‑18 and tumor necrosis factor‑α, and increased the expression of CD31, smooth muscle (SM) α‑actin and SM‑myosin heavy chain.