RESUMO
Objective:To explore the value and significance of transcranial color-coded duplex (TCCD) parameters, serum insulin-like growth factor-1 (IGF-1), neuron-specific enolase (NSE) levels in the evaluation of the condition of cerebral infarction.Methods:One hundred and ten patients with cerebral infarction in Anhui Wanbei Coal-Electricity Group General Hosptial were selected from April 2018 to February 2020, and TCCD examination was performed after admission. Blood samples were taken to determine the levels of serum IGF-1 and NSE, and corresponding treatment was given. The TCCD parameters and serum IGF-1 and NSE levels were compared in patients with different disease severity, plaque nature and different prognosis after 3 months′ follow-up. The correlation between the above indicators and the condition and plaque nature and the predictive value of the prognosis of patients with cerebral infarction were analyzed.Results:The level of IGF-1 were negatively correlated with the severity of disease ( r=- 0.650) and the nature of plaques ( r=- 0.711); and the level of NSE and resistance index (RI), pulsatility index (PI) were positively correlated with the severity of the disease ( r=0.609, 0.613, 0.645) and the nature of plaques ( r=0.589, 0.579, 0.608), and the differences were statistically significant ( P<0.05). After 3 months′ follow-up, the level of IGF-1 in the favourable prognosispatients was higher than that in the unfavourable prognosis patients, the levels of NSE, RI and PI in the favourable prognosis patients were lower than those in the unfavourable prognosis patients: (9.01 ± 2.64) μg/L vs. (25.13 ± 3.82) μg/L, 1.05 ± 0.19 vs. 1.32 ± 0.22, 0.69 ± 0.06 vs. 0.89 ± 0.07, and the differences were statistically significant ( P<0.05). The area under the curve (AUC) of RI, PI, IGF-1 and NSE in predicting the prognosis of cerebral infarction was less than that of combined diagnosis. Conclusions:The early use of TCCD parameters, serum IGF-1 and NSE combined detection can provide evidence-based guidance for evaluating the condition and prognosis of cerebral infarction.
RESUMO
The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulation-induced pancreatic acinar cellular injury and trypsinogen activation or NF-kappaB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-kappaB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10(-3) mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P 0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-kappaB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.
Assuntos
Carbacol/farmacologia , Agonistas Colinérgicos/farmacologia , NF-kappa B/metabolismo , Pâncreas/metabolismo , Pâncreas/patologia , Ratos Wistar , Receptor Muscarínico M3/agonistas , Tripsinogênio/metabolismoRESUMO
The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulationinduced pancreatic acinar cellular injury and trypsinogen activation or NF-κB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-κB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10-3 mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P ＜0.01) following the treatment with a high concentration of carbachol (10-3 mol/L) in vitro. The addition of 10-2 mol/L PDTC didn't result in a significant decrease in the activity of trypsin and the leakage of LDH from pancreatic acinar cells treated with a high concentration of carbachol (10-3 mol/L) in vitro (P＞0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-κB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.