Erythropoietin alleviates lung ischemia-reperfusion injury by activating the FGF23/FGFR4/ERK signaling pathway.

Background: The purpose of the present study was to investigate the effect of erythropoietin (EPO) on lung ischemia-reperfusion injury (LIRI). Methods: Sprague Dawley rats and BEAS-2B cells were employed to construct an ischemia-reperfusion (I/R)-induced model in vivo and in vitro, respectively. Afterward, I/R rats and tert-butyl hydroperoxide (TBHP)-induced cells were treated with different concentrations of EPO. Furthermore, 40 patients with LIRI and healthy controls were enrolled in the study. Results: It was observed that lung tissue damage, cell apoptosis and the expression of BAX and caspase-3 were higher in the LIRI model in vivo and in vitro than in the control group, nevertheless, the Bcl-2, FGF23 and FGFR4 expression level was lower than in the control group. EPO administration significantly reduced lung tissue damage and cell apoptosis while also up-regulating the expression of FGF23 and FGFR4. Rescue experiments indicated that EPO exerted a protective role associated with the FGF23/FGFR4/p-ERK1/2 signal pathway. Notably, the expression of serum EPO, FGF23, FGFR4 and Bcl-2 was decreased in patients with LIRI, while the expression of caspase-3 and BAX was higher. Conclusion: EPO could effectively improve LIRI, which might be related to the activation of the FGF23/FGFR4/p-ERK1/2 signaling pathway.

Gigantol ameliorates DSS-induced colitis via suppressing ß2 integrin mediated adhesion and chemotaxis of macrophage.

ETHNOPHARMACOLOGICAL RELEVANCE: Dendrobium, recognized as "Shihu" in traditional Chinese medicine, holds a rich history of medicinal utilization documented in the Chinese Pharmacopoeia. Ancient texts like "Shen Nong Ben Cao Jing" extol Dendrobium's virtues as a superior herbal medicine fortifying "Yin" and invigorating the five viscera. Dendrobium is extensively employed for the treatment of gastrointestinal inflammatory disorders, showcasing significant therapeutic efficacy, particularly against ulcerative colitis (UC), within the realm of Chinese ethnopharmacology. Dendrobium plays crucial pharmacological roles due to its rich content of polysaccharides, alkaloids, phenanthrenes, and bibenzyls. Gigantol, a prominent bibenzyl compound, stands out as one of the most vital active constituents within Dendrobium, the gigantol content of Dendrobium leaves can reach approximately 4.79 µg/g. Its significance lies in being recognized as a noteworthy anti-inflammatory compound derived from Dendrobium. AIM OF THE STUDY: Given the pivotal role of gigantol as a primary active substance in Dendrobium, the therapeutic potential of gigantol for gastrointestinal diseases remains enigmatic. Our present investigation aimed to evaluate the therapeutic effects of gigantol on dextran sulfate sodium (DSS)-induced colitis and reveal its potential mechanism in countering UC activity. MATERIALS AND METHODS: The protective efficacy of gigantol against colitis was assessed by examining the histopathological changes and conducting biochemical analyses of colon from DSS-challenged mice. Assessments focused on gigantol's impact on improving the intestinal epithelial barrier and its anti-inflammatory effects in colonic tissues of colitis mice. Investigative techniques included the exploration of the macrophage inflammatory signaling pathway via qPCR and Western blot analyses. In vitro studies scrutinized macrophage adhesion, migration, and chemotaxis utilizing transwell and Zigmond chambers. Furthermore, F-actin and Rac1 activation assays detailed cellular cytoskeletal remodeling. The potential therapeutic target of gigantol was identified and validated through protein binding analysis, competitive enzyme-linked immunosorbent assay (ELISA), cellular thermal shift assay (CETSA), and drug affinity responsive target stability (DARTS) assay. The binding sites between gigantol and its target were predicted via molecular docking. RESULTS: Gigantol ameliorated symptoms of DSS-induced colitis, rectified damage to the intestinal barrier, and suppressed the production of pro-inflammatory cytokines in colonic tissues. Intriguingly, gigantol significantly curtailed NF-κB signaling activation in the colons of DSS-induced colitis mice. Notably, gigantol impaired the ß2 integrin-dependent adhesion and migratory capacity of RAW264.7 cells. Moreover, gigantol notably influenced the cytoskeleton remodeling of RAW264.7 cells by suppressing Vav1 phosphorylation and Rac1 activation. Mechanistically, gigantol interacted with ß2 integrin, subsequently diminishing binding affinity with intercellular adhesion molecule-1 (ICAM-1). CONCLUSIONS: In conclusion, these findings elucidate that gigantol ameliorates DSS-induced colitis by antagonizing ß2 integrin-mediated macrophage adhesion, migration, and chemotaxis, thus it may impede macrophage recruitment and infiltration into colonic tissues. This study suggests that gigantol shows promise as a viable candidate for clinical colitis therapy.

Luteolin ameliorates DSS-induced colitis in mice via suppressing macrophage activation and chemotaxis.

OBJECTIVES: Luteolin, known for its multifaceted therapeutic properties against inflammatory diseases, holds potential for addressing the unmet need for effective treatments in ulcerative colitis (UC), a prevalent subtype of inflammatory bowel disease (IBD). This study aimed to comprehensively assess luteolin's therapeutic efficacy in a dextran sulfate sodium (DSS)-induced colitis mouse model, shedding light on its anti-UC mechanisms. METHODS: Our investigation encompassed in vivo assessments of luteolin's therapeutic potential against DSS-induced colitis through rigorous histopathological examination and biochemical analyses. Furthermore, we scrutinized luteolin's anti-inflammatory prowess in vitro using lipopolysaccharide (LPS)-stimulated RAW264.7 cells and primary peritoneal macrophages. Additionally, we quantitatively evaluated the impact of luteolin on C-C motif chemokine ligand 2 (CCL2)-induced macrophage migration employing Transwell and Zigmond chambers. Furthermore, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS) assay, and molecular docking were employed to identify potential therapeutic targets of luteolin and investigate their binding sites and interaction patterns. RESULTS: Luteolin demonstrated therapeutic potential against DSS-induced colitis by ameliorating colitis symptoms, restoring intestinal barrier integrity, and inhibiting proinflammatory cytokine production in the colonic tissues. Moreover, luteolin demonstrated robust anti-inflammatory activity in vitro, in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and primary peritoneal macrophages. Notably, luteolin suppressed the phosphorylation of IKKα/ß, IκBα, and p65, along with preventing IκBα degradation in LPS-treated RAW264.7 cells and peritoneal macrophages. Furthermore, luteolin impaired the migratory behavior of RAW264.7 cells and peritoneal macrophages, as evidenced by reduced migration distance and velocity of luteolin-treated macrophages. Mechanistically, luteolin was found to antagonize IKKα/ß, subsequently inhibiting IKKα/ß phosphorylation and the activation of NF-κB signaling. CONCLUSION: Luteolin emerges as a promising lead compound for the clinical therapy of colitis by virtue of its ability to ameliorate DSS-induced colitis, antagonize IKKα/ß, suppress NF-κB signaling, and impede macrophage activation and migration.

Geniposide ameliorates dextran sulfate sodium-induced ulcerative colitis via KEAP1-Nrf2 signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: The dried fruit of Gardenia jasminoides Ellis (Zhizi in Chinese) is a traditional medicine used for thousands of years in China, Japan and Korea. Zhizi was recorded in Shennong Herbal, as a folk medicine, it reduces fever and treats gastrointestinal disturbance with antiphlogistic effects. Geniposide, an iridoid glycoside, is an important bioactive compound derived from Zhizi and possesses remarkable antioxidant and anti-inflammatory capacities. The pharmacological efficacy of Zhizi is highly related to the antioxidant and anti-inflammatory effects of geniposide. AIM OF THE STUDY: Ulcerative colitis (UC) is a common chronic gastrointestinal disease as a global public health threat. Redox imbalance is an essential factor in the progression and recurrence of UC. This study aimed to explore the therapeutic effect of geniposide on colitis and uncover the underlying mechanisms of geniposide-mediated antioxidant and anti-inflammatory activities. EXPERIMENTAL DESIGN: The study design involved investigating the novel mechanism by which geniposide ameliorates dextran sulfate sodium (DSS)-induced colitis in vivo and lipopolysaccharide (LPS)-challenged colonic epithelial cells in vitro. MATERIALS AND METHODS: The protective effect of geniposide against colitis was evaluated by histopathologic observation and biochemical analysis of colonic tissues in DSS-induced colitis mice. The antioxidant and anti-inflammatory effects of geniposide were evaluated in both DSS-induced colitis mice and LPS-challenged colonic epithelial cells. Immunoprecipitation, drug affinity responsive target stability (DARTS), and molecular docking were performed to identify the potential therapeutic target of geniposide and the potential binding sites and patterns. RESULTS: Geniposide ameliorated the symptoms of DSS-induced colitis and colonic barrier injury, inhibited pro-inflammatory cytokine expression, and suppressed activation of the NF-κB signaling in colonic tissues of DSS-challenged mice. Geniposide also ameliorated lipid peroxidation and restored redox homeostasis in DSS-treated colonic tissues. In addition, in vitro experiments also showed that geniposide exhibited significant anti-inflammatory and antioxidant activity, as evidenced by suppressed IκB-α and p65 phosphorylation and IκB-α degradation, and enhanced the phosphorylation and transcriptional activity of Nrf2 in LPS-treated Caco2 cells. ML385, a specific Nrf2 inhibitor, abolished the protective effect of geniposide against LPS-induced inflammation. Mechanistically, geniposide could bind to KEAP1, thereby disrupting the interaction between KEAP1 and Nrf2, preventing Nrf2 from degradation and activating the Nrf2/ARE signaling pathway, ultimately suppressing the onset of inflammation caused by redox imbalance. CONCLUSIONS: Geniposide ameliorates colitis by activation of Nrf2/ARE signaling, while preventing colonic redox imbalance and inflammatory damage, indicating that geniposide can be considered as a promising lead compound for the treatment of colitis.

Bioactive Compounds from Brown Algae Alleviate Nonalcoholic Fatty Liver Disease: An Extensive Review.

Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases. The increasing NAFLD incidences are associated with unhealthy lifestyles. Currently, there are no effective therapeutic options for NAFLD. Thus, there is a need to develop safe, efficient, and economic treatment options for NAFLD. Brown algae, which are edible, contain abundant bioactive compounds, including polysaccharides and phlorotannins. They have been shown to ameliorate insulin resistance, as well as hepatic steatosis, and all of these biological functions can potentially alleviate NAFLD. Accumulating reports have shown that increasing dietary consumption of brown algae reduces the risk for NAFLD development. In this review, we summarized the animal experiments and clinical proof of brown algae and their bioactive compounds for NAFLD treatment within the past decade. Our findings show possible avenues for further research into the pathophysiology of NAFLD and brown algae therapy.

Inhibition of miR-29b-1-5p Attenuates Inflammatory Response and Pulmonary Fibrosis in LPS-Induced Acute Lung Injury by Regulating RTN4 Expression.

Objective: Acute lung injury (ALI) is a severe respiratory disorder causing alveolar-capillary barrier, leading to a high rate of morbidity and death in critically ill individuals. microRNAs (miRNAs)-mediated mechanism in the pathogenesis of ALI has attracted much interest. Herein, we attempt to characterize a candidate miRNA and its downstream target that is linked to the pathogenesis of ALI. Methods: LPS-conditioned MH-S cells were treated with miR-29a-1-5p mimic, inhibitor, and RNT4 expression vector, and the ALI animal model was injected with agomir and antagomir of miR-29b-1-5p and RNT4 expression vector, in which the pro-inflammatory cytokine production, cell viability and apoptosis, myeloperoxidase (MPO) activity, wet/dry (W/D) ratio, and expression of TGF-ß1, α-smooth muscle actin (α-SMA), E-cadherin, and vimentin were examined. miR-29a-1-5p inhibition of RTN4 translation was confirmed by luciferase activity assays. Results: An elevated miR-29a-1-5p expression was demonstrated in LPS-conditioned MH-S cells. miR-29a-1-5p inhibitor transfection attenuated the production of pro-inflammatory cytokines and MH-S cell viability but enhanced the apoptosis. miR-29a-1-5p inhibition of RTN4 translation was demonstrated in the setting of LPS-induced ALI. LPS-induced murine models demonstrated upregulated miR-29a-1-5p. Intravenous injection of miR-29b-1-5p agomir attenuated mouse lung injury and pulmonary fibrosis. RTN4 overexpression resisting to miR-29a-1-5p overexpression was demonstrated in LPS-induced murine models. Conclusion: The findings obtained from the study that disturbing the action of miR-29a-1-5p may be a novel therapeutic strategy for preventing ALI.

Zeaxanthin attenuates OVA-induced allergic asthma in mice by regulating the p38 MAPK/ß-catenin signaling pathway.

BACKGROUND: Asthma is a heterogeneous and complex chronic airway disease with a high incidence rate, characterized by chronic airway inflammation. Although the anti-inflammatory effect of zeaxanthin has been demonstrated in various disease models, its explicit role in allergic asthma remains elusive. METHODS: An allergic asthma model was established by ovalbumin (OVA) stimulation in BALB/c nude mice. The pathological examination, collagen deposition and expression of α-smooth muscle actin (α-SMA) in lung tissues were determined by hematoxylin and eosin (H&E), MASSON and immunofluorescence staining, respectively. Besides, the effect of zeaxanthin on inflammation and oxidative stress was assessed by the enzyme-linked immunosorbent assay (ELISA) and spectrophotometry measure. Moreover, the underlying mechanism was analyzed by detecting the expression of phosphorylated p38 (p-p38), p38, ß-catenin, p-c-Jun N-terminal kinase (p-JNK) and JNK with western blot assays. RESULTS: The distinct infiltration of inflammatory cells was observed in the OVA-induced asthma mice model with significantly increased concentrations of immunoglobulin E (IgE), interleukin-4 (IL-4), IL-5, IL-13 and eotaxin (p˂0.001), which were prominently reversed by zeaxanthin treatment (p˂0.001). In addition, zeaxanthin treatment decreased the OVA-induced collagen deposition and α-SMA expression. A similar inhibitory effect of zeaxanthin on the oxidative stress was also observed in the OVA-induced asthma mice model, as evidenced by the prominent decrease of malondialdehyde (MDA) concentration and the remarkable increase of superoxide dismutase (SOD), glutathione S transferase (GST) and Glutathione (GSH) concentrations (p˂0.001). Moreover, zeaxanthin introduction markedly reduced the relative expressions of p-p38/p38, ß-catenin and p-JNK/JNK in the OVA-induced asthma mice model (p˂0.001), indicating that zeaxanthin suppressed the p38 mitogen-activated protein kinase (p38 MAPK)/ß-catenin signaling pathway in the OVA-induced asthma mice model. CONCLUSIONS: Zeaxanthin attenuated OVA-induced allergic asthma in mice via modulating the p38 MAPK/ß-catenin signaling pathway.

TRIM50 Inhibits Proliferation and Metastasis of Gastric Cancer via Promoting ß-Catenin Degradation.

Background: Gastric cancer (GC) is a common malignancy with a poor prognosis. Tripartite motif-containing 50 (TRIM50) belongs to the TRIM family and is reported to be related to numerous cancers. This study aimed to investigate the function of TRIM50 in GC. Methods: Three microarray datasets (GSE13911, GSE79973, and GSE19826) containing GC and adjacent nontumor tissues were used for bioinformatics analysis to screen GC-related genes and assess the associations between GC development and TRIM50 expression. Then, TRIM50 expression in GC cells was detected at mRNA and protein levels. After TRIM50 was knockdown or overexpressed, the effect of TRIM50 on the proliferation and metastasis of GC cells was analyzed using Cell Counting Kit-8 (CCK-8), flow cytometry, scratch, and Transwell assays. The interaction between TRIM50 and ß-catenin was analyzed. The expression of cell cycle-, migration-, invasion-, and Wnt/ß-catenin signaling pathway-related proteins was detected by Western blot. Furthermore, we measured the role of TRIM50 overexpression on tumor growth as well as the Wnt/ß-catenin signaling pathway in vivo. In addition, XAV939 (a WNT/ß-catenin signaling pathway inhibitor) was used to clarify the mechanism of TRIM50 on GC. Results: Bioinformatics revealed that TRIM50 expression was decreased in GC samples and associated with GC development. In vitro study revealed that TRIM50 overexpression impeded the GC cell proliferation and metastasis, while TRIM50 knockdown presented the opposite results. In addition, TRIM50 interacted with ß-catenin to induce the degradation of ß-catenin. In in vivo assay, TRIM50 overexpression inhibited tumor growth and blocked the Wnt/ß-catenin signaling pathway. In addition, TRIM50 knockdown-promoted cell proliferation and metastasis in GC cells were inverted by XAV939. Conclusion: TRIM50 overexpression may inhibit cell proliferation and metastasis in GC via ß-catenin degradation, indicating that TRIM50 could be a target for the treatment of GC.

IL-4-C-590T locus polymorphism and susceptibility to asthma in children: a meta-analysis

Abstract Objectives The study aimed to evaluate the link between the IL-4-C590T polymorphism and asthma susceptibility in children by meta-analysis. Sources The study collected all the case-control studies found in PubMed, Embase, CNKI, Wanfang, VIP, and other databases until September 2019. Stata v. 15.0 was used to conduct meta-analysis, calculate the combined OR and its 95% CI, and then conduct subgroup analysis. Summary of the findings Seven studies were included in the study, containing 860 cases and 810 controls. Relative to the C allele, the T allele at the IL-4-C590T locus was associated with susceptibility to asthma in children (OR = 1.45, 95% CI: 1.05-2.01). The results of ethnicity subgroup analysis showed that there was statistical significance, with OR = 1.61 (95% CI: 1.01-2.57) in the Asian population. In the dominant and recessive genetic models, the overall test and the Asian population subgroup analysis were statistically significant. In the homozygous model, there was statistical significance, but no statistical significance in heterozygous model. Conclusions The IL-4-C590T polymorphism was associated with asthma susceptibility, and T allele and TT genotype may increase the risk of asthma susceptibility in children, especially in the Asian population.

Knockdown of ZNF479 inhibits proliferation and glycolysis of gastric cancer cells through regulating ß-catenin/c-Myc signaling pathway.

Gastric cancer is the fifth most common malignancy and the third most deadly tumor in the world. Zinc finger protein 479 (ZNF479) has been demonstrated to play crucial roles in hepatocellular carcinoma. However, the function of ZNF479 in gastric cancer remains to be clarified. The current study aimed to investigate the role of ZNF479 in gastric cancer progression and elucidate the potential molecular mechanism. In this study, Cell Count Kit-8 and colony formation assays demonstrated that knockdown of ZNF479 inhibited cell proliferation in AGS and SGC-7901 cells. Of note, knockdown of ZNF479 hinders tumor growth of xenograft tumor mice. What is more, knockdown of ZNF479 inhibited glucose uptake, lactate production, adenosine triphosphate level, and extracellular acidification ratio; increased oxygen consumption ratio in gastric cancer cells; and decreased the expression of glycolytic proteins both in vitro and in vivo. Furthermore, analysis mechanism suggests that ZNF479 participated in the regulation of gastric cancer progression through affecting the ß-catenin/c-Myc signaling pathway. Collectively, ZNF479 plays a role as an oncogene through modulating ß-catenin/c-Myc signaling pathway in the development of gastric cancer, which provides a new research target for future studies.

UCH-L3 promotes non-small cell lung cancer proliferation via accelerating cell cycle and inhibiting cell apoptosis.

Ubiquitin C-terminal hydrolase-L3 (UCH-L3) is a deubiquitinase that has a crucial role in oncogenesis. This study was aimed to explore the biological function of UCH-L3 in non-small cell lung cancer (NSCLC). Bioinformatics analysis was used to detect UCH-L3 expression in NSCLC tissues and normal lung tissues, and to analyze the relationship between UCH-L3 expression and survival of patients. qRT-PCR and western blotting assays were used to detect UCH-L3 expression in NSCLC tumor tissues and adjacent normal tissues. CCK-8 assay was performed to examine the effect of UCH-L3 on NSCLC cell proliferation. Flow cytometry assay was conducted to examine the effect of UCH-L3 on NSCLC cell cycle and apoptosis. The expression of UCH-L3 in NSCLC tissues was markedly higher than in normal lung tissues, and high expression of UCH-L3 was positively associated with the poor survival of patients. UCH-L3 knockdown significantly inhibited the proliferation of NSCLC cells, whereas UCH-L3 overexpression had the opposite effect. Moreover, UCH-L3 promoted NSCLC cells proliferation via accelerating cell cycle and inhibiting cell apoptosis. UCH-L3 is upregulated in NSCLC and positively associated with the poor survival, and its expression contributes to NSCLC cell proliferation by accelerating cell cycle and inhibiting cell apoptosis.

IL-4-C-590T locus polymorphism and susceptibility to asthma in children: a meta-analysis.

OBJECTIVES: The study aimed to evaluate the link between the IL-4-C590T polymorphism and asthma susceptibility in children by meta-analysis. SOURCES: The study collected all the case-control studies found in PubMed, Embase, CNKI, Wanfang, VIP, and other databases until September 2019. Stata v. 15.0 was used to conduct meta-analysis, calculate the combined OR and its 95% CI, and then conduct subgroup analysis. SUMMARY OF THE FINDINGS: Seven studies were included in the study, containing 860 cases and 810 controls. Relative to the C allele, the T allele at the IL-4-C590T locus was associated with susceptibility to asthma in children (OR = 1.45, 95% CI: 1.05-2.01). The results of ethnicity subgroup analysis showed that there was statistical significance, with OR = 1.61 (95% CI: 1.01-2.57) in the Asian population. In the dominant and recessive genetic models, the overall test and the Asian population subgroup analysis were statistically significant. In the homozygous model, there was statistical significance, but no statistical significance in heterozygous model. CONCLUSIONS: The IL-4-C590T polymorphism was associated with asthma susceptibility, and T allele and TT genotype may increase the risk of asthma susceptibility in children, especially in the Asian population.

Emodin protects against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway.

OBJECTIVE: Our aim was to investigate the effect of emodin on intestinal and lung injury induced by acute intestinal injury in rats and explore potential molecular mechanisms. METHODS: Healthy male Sprague-Dawley (SD) rats were randomly divided into five groups (n=10, each group): normal group; saline group; acute intestinal injury model group; model + emodin group; model+NF-κB inhibitor pynolidine dithiocarbamate (PDTC) group. Histopathological changes in intestine/lung tissues were observed by Hematoxylin and Eosin (H&E) and terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling (TUNEL) staining. Serum IKBα, p-IKBα, surfactant protein-A (SP-A) and toll-like receptor 4 (TLR4) levels were examined using enzyme-linked immunosorbent assay (ELISA). RT-qPCR was performed to detect the mRNA expression levels of IKBα, SP-A and TLR4 in intestine/lung tissues. Furthermore, the protein expression levels of IKBα, p-IKBα, SP-A and TLR4 were detected by Western blot. RESULTS: The pathological injury of intestinal/lung tissues was remarkedly ameliorated in models treated with emodin and PDTC. Furthermore, the intestinal/lung injury scores were significantly decreased after emodin or PDTC treatment. TUNEL results showed that both emodin and PDTC treatment distinctly attenuated the apoptosis of intestine/lung tissues induced by acute intestinal injury. At the mRNA level, emodin significantly increased the expression levels of SP-A and decreased the expression levels of IKBα and TLR4 in intestine/lung tissues. According to ELISA and Western blot, emodin remarkedly inhibited the expression of p-IKBα protein and elevated the expression of SP-A and TLR4 in serum and intestine/lung tissues induced by acute intestinal injury. CONCLUSION: Our findings suggested that emodin could protect against intestinal and lung injury induced by acute intestinal injury by modulating SP-A and TLR4/NF-κB pathway.

Safety and efficacy analysis of DEB-TACE treatment in elderly patients with hepatocellular carcinoma: a comparative cohort study.

The aim of this study was to explore the difference of liver function change, safety profiles and efficacy of drug-eluting bead transarterial chemoembolization (DEBTACE) therapy between elderly and middle-aged hepatocellular carcinoma (HCC) patients. 91 HCC patients were enrolled in this prospective cohort study. They were treated by DEB-TACE therapy and divided into elderly group (age >= 65 years, n=30) and middle-aged group (age < 65 years, n=61), liver function, safety profiles and treatment response were recorded. No difference of liver function was found between two groups before operation and at 1 week post DEB-TACE treatment. While the portion of abnormal total protein (TP) in elderly group was elevated than that in middleage group at 1-3 months after operation. During operation, elderly group presented with raised incidence of vomiting compared with middle-aged group, whereas elderly patients displayed lower incidence of pain than middle-aged patients at 1 month post treatment. No other difference of safety profiles was found between the two groups. At 1-3 months after treatment, elderly patients achieved complete response (CR) of 26.7% and overall response rate (ORR) of 93.3%, meanwhile, middle-aged patients obtained CR of 23.0% and ORR of 90.2%. No difference of CR and ORR was found between elderly and middle-aged patients, in addition, no difference of OS was observed between the two groups. In conclusion, DEB-TACE therapy was well tolerated in elderly HCC patients, and it possessed equal efficacy in elderly patients compared with middle-aged patients.

[ARTICLE WITHDRAWN] miR-630 Inhibits Epithelial-to-Mesenchymal Transition (EMT) by Regulating the Wnt/ß-Catenin Pathway in Gastric Cancer Cells.

THIS ARTICLE WAS WITHDRAWN BY THE PUBLISHERS IN NOVEMBER 2020.