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1.
Int J Biol Markers ; 33(3): 308-313, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29683068

RESUMO

BACKGROUND: CD44 has recently been reported as a biomarker for pancreatic cancer. However, the predictive value of CD44 in pancreatic cancer remains controversial. Therefore, we performed this meta-analysis to evaluate the association between the expression of CD44 and clinicopathological features, and the outcome of pancreatic cancer patients. MATERIALS AND METHOD: A comprehensive literature search was performed using PubMed, Embase, and Chinese National Knowledge Infrastructure. The statistical analysis was conducted using Stata software. RESULTS: A total of nine studies including 583 cases were included in this meta-analysis. The meta-analysis indicated that CD44 overexpression was associated with poor five-year overall survival rate (OR 0.52; 95% CI 0.30, 0.91; P = 0.02), more lymph node invasion (OR 3.14 (positive vs. negative); 95% CI 1.47, 6.73; P = 0.003), more advanced T stage (OR 2.4 (T3,4 vs. T1,2); 95% CI 1.28, 4.52; P = 0.007), and more advanced TNM stage (OR 4.53 (III~IV vs. I~II); 95% CI 1.46, 14.08; P = 0.01). However, CD44 overexpression was not associated with other clinicopathological features, such as tumor size, differentiation, and distance metastasis. CONCLUSIONS: The current evidence suggests that CD44 is an efficient prognostic factor in pancreatic cancer.


Assuntos
Biomarcadores Tumorais/genética , Receptores de Hialuronatos/genética , Neoplasias Pancreáticas/genética , Prognóstico , Intervalo Livre de Doença , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Linfonodos/patologia , Metástase Linfática , Masculino , Estadiamento de Neoplasias , Neoplasias Pancreáticas/patologia
2.
World J Emerg Med ; 8(1): 61-64, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28123623

RESUMO

BACKGROUND: The study aimed to investigate the therapeutic benefits of intravenous Xuebijing on acute kidney injury (AKI) in rats with paraquat intoxication. METHODS: Male Sprague-Dawley rats were randomly divided equally into three groups: sham group (n=8), paraquat group (n=8) and Xuebijing-treated group (n=8) using a random number table. The rats were intraperitoneally injected with 50 mg/kg of paraquat. One hour after paraquat administration, the rats were treated intravenously with Xuebijing (8 mL/kg). At 12 hours after paraquat administration, serum was collected to evaluate kidney function, then the rats were sacrificed and kidney samples were immediately harvested. AKI scores were evaluated by renal histopathology and pro-inflammatory cytokines mRNA levels in kidney were assayed using real-time RT-PCR. RESULTS: Serum urea nitrogen, creatinine and AKI scores were significantly higher in the paraquat group, compared with the sham group (P<0.05, respectively). Moreover, interleukin (IL)-1ß, IL-6 and TNF-α mRNA levels were significantly higher in the paraquat group (P<0.01, respectively). However, intravenous Xuebijing significantly decreased serum urea nitrogen, creatinine, AKI scores and IL-1ß, IL-6 and TNF-α mRNA levels, compared with the paraquat group (P<0.05, respectively). CONCLUSION: Intravenous Xuebijing attenuates AKI following paraquat poisoning by suppressing inflammatory response.

3.
Artigo em Inglês | WPRIM (Pacífico Ocidental) | ID: wpr-789789

RESUMO

@#BACKGROUND: The study aimed to investigate the therapeutic benefits of intravenous Xuebijing on acute kidney injury (AKI) in rats with paraquat intoxication. METHODS: Male Sprague-Dawley rats were randomly divided equally into three groups:sham group (n=8), paraquat group (n=8) and Xuebijing-treated group (n=8) using a random number table. The rats were intraperitoneally injected with 50 mg/kg of paraquat. One hour after paraquat administration, the rats were treated intravenously with Xuebijing (8 mL/kg). At 12 hours after paraquat administration, serum was collected to evaluate kidney function, then the rats were sacrificed and kidney samples were immediately harvested. AKI scores were evaluated by renal histopathology and pro-inflammatory cytokines mRNA levels in kidney were assayed using real-time RT-PCR. RESULTS: Serum urea nitrogen, creatinine and AKI scores were significantly higher in the paraquat group, compared with the sham group (P<0.05, respectively). Moreover, interleukin (IL)-1β, IL-6 and TNF-α mRNA levels were significantly higher in the paraquat group (P<0.01, respectively). However, intravenous Xuebijing significantly decreased serum urea nitrogen, creatinine, AKI scores and IL-1β, IL-6 and TNF-α mRNA levels, compared with the paraquat group (P<0.05, respectively). CONCLUSION: Intravenous Xuebijing attenuates AKI fol owing paraquat poisoning by suppressing inflammatory response.

4.
Toxicol Mech Methods ; 26(1): 32-5, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-26313688

RESUMO

CONTEXT: Paraquat exposure commonly occurs in the developing countries and the mortality rate is high. However, there is currently no consensus on the efficacy of treatment for paraquat exposure. OBJECTIVE: The study was aimed to explore the effects of tumor necrosis factor-α (TNF-α) induced protein 6 (TSG-6) on acute lung injury (ALI) following paraquat exposure in rats. MATERIALS AND METHODS: Male Sprague-Dawley (SD) rats were randomly divided into the sham group (n = 8), the paraquat group (n = 8), and the paraquat TSG-6-treated group (n = 8). Rats were administered with 50 mg/kg of paraquat intraperitoneally. At 1 h after exposure, rats were treated with 30 µg of recombinant human TSG-6 (rhTSG-6) intraperitoneally. After 6 h of exposure, ALI scores were evaluated by histology and the expression of pro-inflammatory cytokines in lung was assayed using real-time RT-PCR. RESULTS: ALI scores were significantly lower in the paraquat TSG-6-treated group, compared with the paraquat group (p < 0.05). The expression of interleukin (IL)-1ß, IL-6, and TNF-α mRNA was significantly lower in the paraquat TSG-6-treated group, compared with the paraquat group (p < 0.01, respectively). DISCUSSION AND CONCLUSION: Administration of rhTSG-6 attenuates ALI following paraquat exposure by suppressing inflammatory response.


Assuntos
Lesão Pulmonar Aguda/induzido quimicamente , Moléculas de Adesão Celular/farmacologia , Regulação da Expressão Gênica/efeitos dos fármacos , Paraquat/toxicidade , Proteínas Recombinantes/farmacologia , Lesão Pulmonar Aguda/tratamento farmacológico , Animais , Moléculas de Adesão Celular/administração & dosagem , Citocinas/genética , Citocinas/metabolismo , Pulmão/metabolismo , Masculino , Ratos , Ratos Sprague-Dawley , Proteínas Recombinantes/administração & dosagem
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