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Patients who are bedridden are for a long-time prone to develop bedsores, especially in the hip and sacral areas and limbs, which causes eczema, ulcers, infection and other complications, resulting in pain and more medical costs. Therefore, the medical staff of the Second Affiliated Hospital of Zunyi Medical University designed and developed a kind of anti-bedsore turning pad, and has obtained the national utility model patent (ZL 2021 2 3004923.9), which is suitable for various long-term bedridden patients. The anti-bedsore turning pad includes the center axis of the turning pad, and ventilation pad 1 and ventilation pad 2 designed on the left and right of turning pad center axis. Under the ventilation pad 1 and the ventilation pad 2, the air pad 1 and the air pad 2 are respectively designed. There is a bedspread connected with ventilation pad 1 and ventilation pad 2 on the inflatable pad 1 and the inflatable pad 2. Through the design of inflatable pad 1 and inflatable pad 2, the left and right of the anti-bedsore turning pad can be lowered or raised independently, which is convenient for the patient's body to tilt and turn over, and can significantly reduce the number of nursing staff and the burden of nursing staff when turning over. In addition, it is convenient to replace the force site at any time and reduce the occurrence of pressure ulcers caused by long-term pressure on the force site. Through the design of ventilation cushion 1 and ventilation cushion 2, the internal gas flow of the turning pad can be made, and the ventilation between the patient and the turning pad can be kept dry, so as to reduce the occurrence of eczema, ulcers or infection and other complications, and ultimately reduce the occurrence of bedsores. In addition, through the design of the most superficial limb pad, the patient's limb can be appropriately elevated or massaged, which increases the comfort of the patient. The anti-bedsore turning pad is simple and effective, and can be widely used in long-term bedridden patients.
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Humans , Pressure Ulcer/epidemiology , Ulcer , Respiration , Risk Factors , EczemaABSTRACT
Objective:To investigate whether microRNA-21-5p (miR-21-5p) alleviates hyperoxia-induced acute lung injury (HALI) through activating the phosphatidylinositol 3 kinase/serine-threonine protein kinase (PI3K/Akt) signaling pathway by regulating apoptosis of type Ⅱ alveolar epithelial cell (AECⅡ).Methods:Seventy-two male Sprague-Dawley (SD) rats were divided into normozone-controlled group, HALI group, PI3K/Akt signaling pathway inhibitor LY294002+HALI group (LY+HALI group), miR-21-5p overexpression+LY294002+HALI group (miR-21-5p+LY+HALI group), miR-21-5p overexpression+HALI group (miR-21-5p+HALI group), and dimethyl sulfoxide (DMSO)+HALI group by random number table method with 12 rats in each group. Animal models of HALI were prepared using 95% concentrations of oxygen. The animals in the normozone-controlled group were fed normally under normoxia. Transfection of lung tissue by miR-21-5p adeno-associated viral vector AAV6-miR-21-5p was performed by instillation of 200 μL titer (1×10 12 TU/mL) through a tracheal catheter 3 weeks prior to modeling. DMSO and LY294002 were administered via the tail vein at 0.3 mg/kg 1 hour before modeling. After 48 hours of modeling, carotid artery blood was collected to detect oxygenation index (OI) and respiratory index (RI), and real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect miR-21-5p expression. Lung tissue was collected, and the levels of inflammatory factors including tumor necrosis factor-α (TNF-α) and interleukins (IL-6, IL-1β) were measured by enzyme-linked immunosorbent assay (ELISA), and the ratio of pulmonary wet/dry weight (W/D) was determined, and the pathological changes of lung histopathology were observed under the light microscopy after hematoxylin-eosin (HE) staining. Each group was purified AECⅡ cells from 6 rats, the apoptosis rate was detected by flow cytometry, and the expression levels of phosphatase and tensin homologous gene (PTEN), and proteins from the PI3K/Akt signaling pathway were detected by Western blotting. Results:Compared with the normozone-controlled group, alveolar septal thickening and massive inflammatory cell infiltration were found after hyperoxia exposure, RI, inflammatory factors, lung W/D ratio, pathological score, AECⅡ cells early apoptosis rate, PTEN protein expression and phosphorylation level of Akt were increased, while OI and miR-21-5p expression were decreased, indicating the successful preparation of the model. After pretreatment, LY294002 could aggravate the pathological injury of lung tissue in HALI rats, RI, inflammatory factors and lung W/D ratio were further increased, and OI was further reduced compared with HALI group. At the same time, it could promote the AECⅡ cell apoptosis, further up-regulate the expression of PTEN, and reduce the phosphorylation of Akt. However, miR-21-5p pretreatment could negatively regulate PTEN, activate PI3K/Akt signal pathway, inhibit AECⅡ cell apoptosis, and reduce HALI, which was shown by the decreased level of inflammatory factors in miR-21-5p+LY+HALI group compared with LY+HALI group [TNF-α (μg/L): 100.33±3.48 vs. 116.55±2.53, IL-6 (ng/L): 141.06±3.70 vs. 161.31±3.59, IL-1β (μg/L): 90.82±3.69 vs. 112.23±2.87, all P < 0.05], RI, lung injury pathology score, lung W/D ratio, and AECⅡ cell early apoptosis rate were significantly decreased [RI: 0.81±0.02 vs. 1.05±0.07, pathology score: 0.304±0.008 vs. 0.359±0.007, lung W/D ratio: 5.29±0.03 vs. 5.52±0.08, apoptosis rate: (27.20±2.34)% vs. (34.17±1.49)%, all P < 0.05], OI and expressions of miR-21-5p were significantly increased [OI (mmHg, 1 mmHg≈0.133 kPa): 266.71±2.75 vs. 230.12±4.04, miR-21-5p (2 -ΔΔCt): 2.21±0.13 vs. 0.33±0.03, both P < 0.05], and PTEN protein expression in AECⅡ cell was significantly reduced (PTEN/GAPDH: 0.50±0.06 vs. 0.93±0.06, P < 0.05), and phosphorylation level of Akt was significantly increased [phosphorylated Akt (p-Akt) protein (p-Akt/GAPDH): 0.86±0.05 vs. 0.56±0.06, P < 0.05]. Conclusion:miR-21-5p attenuates HALI by inhibiting AECⅡ cell apoptosis, possibly through negative regulation of PTEN to activate PI3K/Akt signaling pathway.
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Mitophagy is the selective degradation of damaged mitochondria, and it is of great significance to maintain the normal quantity and quality of mitochondria to ensure cell homeostasis and survival. Necroptosis is a type of programmed cell necrosis that can be induced by excessive mitophagy. Reactive oxygen species (ROS) are produced mainly by mitochondria and can damage mitochondria. Hyperoxic acute lung injury (HALI) is a serious complication of clinical oxygen therapy, and its pathogenesis is not clear. Existing studies have shown that mitophagy and necroptosis are involved in the occurrence of HALI. There are many mechanisms regulating mitophagy and necroptosis, including tumor necrosis factor-α (TNF-α), E3 ubiquitin protein ligase (PINK1/Parkin) protein pathway encoded by PTEN-induced kinase 1/PARK2 gene, phosphoglycerate mutase 5 (PGAM5), etc. PGAM5 has been proved to be a key factor linking mitophagy and necroptosis. Previous studies of our team found that the mechanism of microRNA-21-5p (miR-21-5p) alleviating HALI was related to its pGAM5-mediated inhibition of mitophagy, but the mechanism of PGAM5-mediated mitophagy and necroptosis remains unclear. Therefore, this paper reviews the targets of PGAM5-mediated mitophagy and necroptosis, in order to find clues of lung protection of pGAM5-mediated mitophagy and necroptosis in HALI, and provide theoretical basis for subsequent basic research.
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Objective To investigate the effects of agmatine (AGM) on the apoptosis of type Ⅱ alveolar epithelial cells (AECⅡ) in rats with hyperoxia-induced acute lung injury (HALI) and provide a theoretical basis for the treatment of HALI. Methods A total of 24 Sprague-Dawley (SD) rats were randomly divided into three groups:normal control group (fed in air), HALI model group and AGM pretreatment group (400 mg/kg AGM was given before the hyperoxia treatment or HALI model establishment), each group with 8 rats. The rats were placed in a self-made high oxygen model box with oxygen concentration of > 90%, temperature of 25-27 ℃, humidity of 50%-70% and carbon dioxide concentration < 0.5% to replicate the HALI rat model; no any treatment was given to the normal control group. After the hyperoxia was treated for 48 hours, the arterial blood was taken from the rat carotid artery for blood gas analysis;under light microscope, the pathological changes of lung tissues were observed and the pathological evaluation scores were carried out; the contents of tumor necrosis factor-α (TNF-α) and interleukins (IL-6, IL-1) in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA); the apoptosis of AECⅡ of lung tissues was determined by flow cytometry, and the apoptotic rate was calculated; the expressions of the apoptosis related protein Bcl-2 and Bax were detected by Western Blot. Results Compared with the normal control group, the oxygenation index (OI) and Bcl-2 of HALI model group and AGM pretreatment group were significantly decreased [OI (mmHg, 1mmHg = 0.133 kPa): 135.04±16.82 vs. 463.74±22.04, Bcl-2 protein expression (A value): 0.35±0.18 vs. 0.89±0.08], while the respiratory index (RI), pathological scores of lung injury, TNF-α, IL-6, IL-1, the apoptosis rate of AECⅡ, Bax protein expression were all significantly increased [RI: 1.29±0.15 vs. 0.24±0.03, pathological score of lung tissue: 4.72±1.32 vs. 0, TNF-α (μg/L): 44.48±1.42 vs. 14.12±0.88, IL-6 (μg/L): 51.46±1.62 vs. 23.20±0.89, IL-1 (μg/L): 44.03±2.45 vs. 11.64±1.34, apoptosis rate of AECⅡ: (56.24±1.14)% vs. (22.64±0.58)%, Bax protein expression (A value): 2.37±0.34 vs. 1.41±0.48, all P < 0.05]. Compared with HALI model group, the OI and Bcl-2 of AGM pretreatment group were significantly increased [OI (mmHg): 364.72±14.56 vs. 135.04±16.82, Bcl-2 protein expression (A value): 0.68±0.10 vs. 0.35±0.18, all P < 0.05], while the RI, pathological scores of lung injury, TNF-α, IL-6, IL-1, apoptosis rate of AECⅡ, and Bax protein expression were significantly decreased [RI: 0.45±0.09 vs. 1.29±0.15, pathological score of lung tissue: 2.30±0.96 vs. 4.72±1.32, TNF-α (μg/L):22.98±0.72 vs. 44.48±1.42, IL-6 (μg/L): 35.79±0.86 vs. 51.46±1.62, IL-1 (μg/L): 24.06±0.86 vs. 44.03±2.45, apoptosis rate of AECⅡ: (28.58±1.21)% vs. (56.24±1.14)%, Bax protein expression (A value): 1.98±0.42 vs. 2.37±0.34, all P < 0.05]. Conclusion The apoptotic rate of AECⅡ in HALI rats is reduced by AGM, and the regulatory mechanism needs to be further studied.
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To investigate the effect of overexpression of microRNA-21-5p (miR-21-5p) on early apoptosis of type Ⅱalveolar epithelial cells (AECⅡ) in rats with hyperoxic acute lung injury (HALI). Methods The Sprague-Dawley (SD) rats were randomly divided into four groups: control group (CON group), hyperoxia group (H group), overexpression group (OE group) and empty vector group (EV group), with 20 rats in each group. HALI animal model was made by inhaling high concentration oxygen (oxygen concentration ≥90%); CON group was arranged to inhale room air. The miR-21-5p adeno-associated virus-6 (AAV-6) overexpression vectors or empty vectors were dripped into the lungs of OE group and EV group through tracheal tube, respectively. The hyperoxia model was prepared after 3 weeks of feeding. At 0, 24, 48 and 60 hours after making model, 5 rats were selected to detect lung injury parameters:oxygenation index (OI), respiratory index (RI), wet/dry ratio (W/D), pathological injury score of lung tissue; real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-21-5p in AECⅡ, and flow cytometry was used to detect the early apoptotic rate of AECⅡ. Results ① The lung injury parameters: in H group, the OI gradually decreased with time, but the RI, lung W/D ratio and pathological score increased gradually with time, the difference between CON group was statistically significant at 24 hours [OI (mmHg, 1 mmHg = 0.133 kPa):336.04±5.79 vs. 400.22±19.70, RI: 0.20±0.02 vs. 0.10±0.06, lung W/D ratio: 5.04±0.09 vs. 4.85±0.09, lung tissue pathological score: 0.13±0.01 vs. 0.07±0.01, all P < 0.05]. It indicated that HALI model could be successfully established by inhaling high concentration oxygen continuously. ② The expression of miR-21-5p: the miR-21-5p was gradually increased in H, OE and EV groups, and the expression of miR-21-5p was significantly higher than that in CON group at 24, 48 and 60 hours. Compared with H group, the expression of miR-21-5p was significantly increased further in OE group at 0, 24, 48 and 60 hours (2-ΔΔCt: 3.75±0.11 vs. 0.98±0.14, 3.98±0.12 vs. 1.18±0.13, 4.28±0.18 vs. 1.49±0.06, 4.66±0.12 vs. 1.80±0.12, all P < 0.05). ③ The early apoptosis of AECⅡ: the early apoptosis rate gradually increased with time in H, OE and EV groups, and the early apoptosis of AECⅡ was significantly higher than that in CON group at 24, 48 and 60 hours. Compared with H group, the early apoptosis rate was significantly decreased in OE group at 24, 48 and 60 hours [(1.22±0.63)% vs. (2.84±0.59)%, (5.76±0.18)% vs. (13.10±2.01)%, (29.48±0.48)% vs. (49.04±1.36)%, all P < 0.05]. ④ There was no significant difference in the expression of miR-21-5p and the early apoptosis of AECⅡ cells between EV group and H group at each time point. Conclusion Overexpression of miR-21-5p could inhibit the early apoptosis of AECⅡ in rats with HALI.
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Autophagy is a fundamental cellular process that plays a role in the turnover of sub-cellular organelles to protein. The activation of autophagy may prevent the pathophysilogical progression of oxidative stress-induced protein damage or organelle damage. The selective form of autophagy can maintain organelle renewal by degrading damaged proteins. In this article, the research progress on the mechanism of autophagy in acute lung injury/acute respiratory distress syndrome (ALI/ARDS) was summarized in order to understand more deeply on this topic and arouse more researchers to pay attention to the role of autophagy in lung protection of ALI/ARDS.
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Objective To investigate the effect of heme oxygenase-1 (HO-1) on the apoptosis of type Ⅱalveolar epithelial cells (AEC-Ⅱ) in rats with hyperoxia-induced acute lung injury (HALI). Methods Twenty-four healthy male Sprague-Dawley (SD) rats were randomly divided into 4 groups (n = 6): control group, HALI group, HO-1 group, and HO-1 inhibition group. The control group was fed in the room air; the HALI group was fed in the hyperoxia box (the oxygen concentration was more than 90%, the temperature was kept at 25-27 ℃, the humidity was maintained at 50%-70%, and the CO2concentration was less than 0.5%); the HO-1 group was fed in the hyperoxia box after HO-1 (0.2 μmol/L) treatment; and the HO-1 inhibition group was fed in the hyperoxia box after treatment with zinc protoporphyrin Ⅸ (20 μmol/L). After 48 hours of hyperoxia treatment, rats were sacrificed, left upper lung tissue was stained with hematoxylin-eosin (HE) and the pathological changes of lung tissue were observed under light microscope. The ratio of wet/dry weight (W/D) was measured in the lower left lung. AECⅡ was extracted from the right lung tissue, the apoptosis rate was detected by flow cytometry, and the expressions of apoptosis-related proteins Bcl-2 and caspase-3 were detected by Western Blot. Results ①It was shown by light microscopy that the lung tissue structure of the control group was clear. In HALI group and HO-1 inhibitor group, the lung tissue structure was disordered, alveolar wall was broken and fused into pulmonary alveoli, alveolar septum was obviously swollen and widened, a large number of inflammatory cells infiltrated, and edema fluid and inflammatory cells appeared in alveolar cavity. The pathological changes of lung tissue in HO-1 group were significantly less than those in HALI group. ② Compared with the control group, the lung W/D ratio, the apoptosis rate of AECⅡand the expression of Bcl-2 protein in the HALI group and the HO-1 inhibitor group were significantly increased, and the expression of caspase-3 was significantly decreased [lung W/D ratio: 4.61±0.41 vs. 3.68±0.45, apoptosis rate of AECⅡ: (42.44±0.93) % vs. (24.74±0.64) %, Bcl-2 (integral absorbance): 0.72±0.18 vs. 0.41±0.12, caspase-3 (integral absorbance): 1.32±0.32 vs. 1.81±0.69, all P < 0.05]. Compared with the HALI group, the lung W/D ratio, the apoptosis rate of AECⅡ, the expression of Bcl-2 protein in HO-1 group were significantly decreased, and the expression of caspase-3 was significantly increased [lung W/D ratio: 3.82±0.28 vs. 4.61±0.41, apoptosis rate of AECⅡ: (26.67±1.58) % vs. (42.44±0.93) %, Bcl-2 (integral absorbance): 0.39±0.08 vs. 0.72±0.18, caspase-3 (integral absorbance): 1.78±0.46 vs. 1.32±0.32, all P < 0.05]. There was no significant difference between HO-1 inhibitor group and HALI group. Conclusions HO-1 can reduce the apoptosis rate of AECⅡin rats with HALI, which may be related to the expressions of apoptosis related proteins Bcl-2 and caspase-3.
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Objective To investigate the influence of continuous veno-venous hemofiltration (CVVH) on cardiac output (CO) value and parameters of hemodynamics monitored by transpulmonary thermodilution technique in critical patients. Methods A prospective cohort study was conduced. Sixty-two critical patients admitted to intensive care unit (ICU) of Zunyi Medical College Affiliated Hospital from January 2011 to October 2015 were enrolled. All of the patients received CVVH through femoral vein puncture catheter. The CO value was monitored before CVVH operation, immediately after CVVH operation (8 ℃ normal saline was injected immediately after the output of blood from the arterial end), 5 minutes after operation, the time at the sudden interruption (press pause key after 10 minutes of operation) and resumed immediately, 15 minutes and 30 minutes after operation by pulse-indicated continuous cardiac output (PiCCO) with transpulmonary thermodilution method. The changes in heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), and blood temperature were observed at all time points. Results From CVVH before start to 5 minutes thereafter, CO values were not significantly changed in patients, fluctuating in 6.96 (7.33, 8.67)-6.98 (6.43, 7.45) L/min. When CVVH was suddenly interrupted, CO value was immediately increased to the peak 8.04 (7.36, 8.77) L/min, which showed statistically significant difference as compared with other time points (all P < 0.01). Immediately after the CVVH recovery from interruption, the CO value dropped to 4.71 (4.14, 7.26) L/min, and it was significantly lower than those at other time points (all P < 0.01). With the CVVH recovery, the patients' CO value was gradually restored to the stable operation ahead of interruption [4.71 (4.14, 7.26)-6.85 (6.08, 7.26) L/min]. During CO monitoring, HR, MAP, CVP and blood temperature of the patients were at the same level, and no significant changes were founded. Conclusions CVVH interruption of immediate PiCCO monitoring CO value were significantly increased, immediately after the CVVH recovery the CO value were significantly reduced, and the normal operation of CVVH did not affect the CO value monitoring. Hemodynamics and blood temperature of all patients were stable during CVVH.
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Objective To explore a simpler, more economic and reproducible method to reproduce a model of high oxygen induced acute lung injury (HALI) in rats. Methods An animal feeding box equipped with a controllable high oxygen was designed. 100 Sprague-Dawley (SD) rats were divided into normal control group and HALI group by random number table method, with 50 rats in each group. Each group was randomly subdivided into five subgroups according to the duration of exposure to high oxygen, namely 0, 24, 48, 72 and 96-hour subgroups, with 10 rats in each subgroup. The rats in normal control group were kept in cages with ambient air, and the rats in HALI group were kept in an oxygen tank in which the oxygen concentration was higher than 90% volume ratio, with the temperature maintained at 25-27 ℃, humidity of 50%-70%, and CO2 concentration 0.05). There were significant differences in changes between 24, 48, 72, and 96 hours as compared with those of the normal control group: OI (mmHg): 24 h 306.19±37.23 vs. 435.65±25.34 and 96 h 245.58±35.25 vs. 465.42±24.75; RI: 24 h 0.31±0.06 vs. 0.24±0.04 and 96 h 0.44±0.03 vs. 0.24±0.06. The same as true in pathological scores of lung tissue: 24 h 0.90±0.74 vs. 0.00±0.00 and 96 h 4.80±1.23 vs. 0.00±0.00; lung W/D ratio: 24 h 4.14±0.46 vs. 3.79±0.44 and 96 h 5.18±0.25 vs. 4.12±0.91, all P < 0.05. Conclusions A self-designed high oxygen box is simple, easy to operate and reproduction of HALI model can be attained. Sustained exposure to high concentrations of oxygen (≥ 90%) for 24 hours can replicate the HALI model successfully, and the most serious injury appears at 48-72 hours after exposure.
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Objective To investigate the effects of microRNA-21-5p (miR-21-5p) on hyperoxic acute lung injury (HALI) in rats and provide a theoretical basis for HALI gene therapy. Methods One hundred and sixty Sprague-Dawley (SD) rats were randomly divided into four groups with number table:hyperoxia control group, phosphate buffer saline (PBS) group, blank virus group and miRNA-21-5p group (each, n = 40). The rats in hyperoxia control group were fed directly in the hyperoxia box (oxygen concentration > 90%); in the other three groups, 200 μL PBS, 200μL slow virus and 200μL miRNA-21-5p slow virus were dropped into the nose respectively, and then they were fed in the hyperoxia box. The rats were exposed to hyperoxia in the boxes for 0, 24, 48 and 72 hours in all the groups, and at each time point, 10 rats were taken randomly from each group to perform arterial blood-gas analysis, calculate oxygenation index (OI) and respiratory index (RI). Afterwards the rats were sacrificed by blood-letting from carotid artery under intra-peritoneal anesthesia, and the lung tissues were obtained to measure the left lung wet/dry weight (W/D) ratio, hemotoxylin-eosin (HE) staining was made and the pathological changes of the right lung were observed under light microscope and the pathological score was measured. Results At 0 hour, the OI, RI, lung W/D ratio and the lung tissue pathology score in rats with hyperoxic injury had no statistically significant differences among the four groups (all P>0.05). With the extension of time, the level of OI was gradually reduced, and the levels of RI, pathologic score and W/D ratio of lung tissues were gradually increased. Compared with the hyperoxia control group, in miRNA-21-5p group, the levels of OI were increased significantly at 24, 48 and 72 hours after the exposure to hyperoxia [mmHg (1 mmHg = 0.133 kPa): 24 hours 358.10±29.25 vs. 306.19±37.23, 48 hours 336.67±29.27 vs. 269.70±29.00, 72 hours 323.81±19.05 vs. 203.81±43.40, all P 0.05). Under the optical microscope, along with the prolongation of exposure to hyperoxia, the structure of alveoli was gradually disturbed, their walls fractured and damaged, alveolar septa widened, edematous, infiltrated with inflammatory cells and in part of the rats a small amount of red blood cell exudates could be seen, but the degree of lung pathological injury in miRNA-21-5p group was much milder than that of the other groups. Conclusion The rat persistently exposed to hyperoxia for 24 hours can establish the rat model of HALI successfully, and the miRNA-21-5p can protect the lung tissue from the damage to some degrees in HALI rats.
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ObjectiveTo study the effect of hydrogen peroxide (H2O2) in inducing apoptosis of typeⅡalveolar epithelial cell (AECⅡ) after overexpression by adenoviral transfection of micro RNA-21-5p (miR-21-5p), and to explore the mechanism of its anti-apoptosis.Methods Subculture AECⅡ were randomly divided into four groups: normal control group (normal saline), H2O2 challenge group ( 0.5 mmol/L H2O2), miR-21-5p overexpression group (miR-21-5p adenovirus+ 0.5 mmol/L H2O2), miR-21-5p negative transfection group (adenovirus void+0.5 mmol/L H2O2). Transmission electron microscopy and flow cytometry were used to detect apoptotic morphology and early apoptotic rate. Real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of miR-21-5p in AECⅡ, and Western Blot was used to detect the protein expressions of Bcl-2, Bax, and caspase-3 at the highest transfection efficiency at different time points (6, 12, 24, 48 hours).Results ① AECⅡ identification: fluorescence microscopy showed the presence of characteristic structure of AECⅡ, i.e. microvilli and osmiophilic lamellar bodies.② Apoptotic morphology: transmission electron microscopy showed cytoplasmic retraction, chromatin condensation, margination, lack of cell surface microvilli, and emptying of osmiophilic lamellar bodies in AECⅡ.③ The expression of miR-21-5p in AECⅡ: the highest transfection efficiency was found at 48 hours. The expression of miR-21-5p in miR-21-5p overexpression group was significantly higher than that of the normal control group, H2O2 challenge group and miR-21-5p negative transfection group (A value: 1.54±0.02 vs. 1.02±0.02, 0.56±0.03, 0.58±0.02, allP< 0.05).④ The rate of early apoptosis: compared with normal control group, the early apoptotic rates in H2O2 challenge group, miR-21-5p negative transfection group and miR-21-5p overexpression group were gradually elevated with the prolongation of injury time. The early apoptotic rate in miR-21-5p overexpression group was significantly lower than that of the H2O2 challenge group and miR-21-5p negative transfection group at all time points except 6 hours [12 hours: (10.73±2.80)% vs. (16.26±0.59)%, (16.04±0.70)%; 24 hours:(16.00±3.44)% vs. (23.29±2.78)%, (23.58±2.31)%; 48 hours: (31.30±3.55)% vs. (50.53±2.17)%, (49.41±1.97)%, allP< 0.05]. There was no significant difference in early apoptotic rate between miR-21-5p negative transfection group and H2O2 challenge group at each time point.⑤ Protein expression: the expressions of Bax and caspase-3 in miR-21-5p overexpression group were significantly lower than those of the H2O2 challenge group and miR-21-5p negative transfection group [Bax (A value): 0.07±0.01 vs. 0.18±0.01, 0.13±0.01; caspase-3 (A value): 0.07±0.01 vs. 0.23±0.01, 0.12±0.01, allP< 0.05], and Bcl-2 protein expression was significantly higher than that of the H2O2 challenge group and miR-21-5p negative transfection group (A value: 0.26±0.01 vs. 0.06±0.01, 0.10±0.01, both P< 0.05).Conclusions① miR-21-5p has the function of anti-apoptosis of AECⅡ.② Adenoviral vector is a successful gene transfer vector when transfected with AECⅡ.③ The anti-apoptosis of AECⅡ by miR-21-5p may be associated with reduced Bax and caspase-3 protein levels and raised expression levels of Bcl-2 protein.