Objective To explore the role and mechanism of mitophagy in ventilator-induced lung injury (VILI) in rats.Methods Thirty-six adult Sprague-Dawley (SD) rats were randomly divided into three groups (eachn = 12): spontaneous breathing group (CON group), normal tidal volume (VT) group (NVT group, VT was 8 mL/kg) and high VT group (HVT group, VT was 40 mL/kg). All rats received endotracheal tube by tracheostomy. The rats in CON group were maintained spontaneous breathing, while those in NVT and HVT groups received mechanical ventilation with corresponding VT. After 4 hours of ventilation, the serum, bronchoalveolar lavage fluid (BALF) and lung tissues were harvested. The lung wet/dry weight (W/D) ratio was assessed, and the histopathology changes were observed by light microscopy, and the ultra structure changes in type Ⅱ alveolar epithelial cell (AECⅡ) were observed by electron microscopy. The levels of interleukin (IL-1β and IL-6) and tumor necrosis factor-α (TNF-α) in serum and BALF were determined by enzyme linked immunosorbent assay (ELISA). The total protein in BALF was measured by bicinchoninic acid methods, and the infiltrated cells in BALF were counted. The mRNA expressions and protein levels of microtube associated light chain 3B (LC3B), mitochondrial DNA coded cytochrome C oxidase Ⅳ (COX-Ⅳ) and nuclear factor-κB p65 (NF-κB p65) in lung tissues were determined by real-time fluorescent quantitation reverse transcription-polymerase chain reaction (RT-qPCR) and Western Blot.Results The histopathology of lung tissue and the ultra structure of AEC Ⅱ were normal in CON group and NVT group, and the obvious inflammatory changes and pathological injury were found in HVT group. Compared with CON and NVT groups, the W/D ratio in HVT group was significantly increased (8.53±1.05 vs. 5.12±0.65, 5.57±0.55, bothP < 0.05), and total protein, infiltrated cells, and IL-1β, IL-6 and TNF-α in BALF were significantly increased [total protein (g/L): 2.35±0.45 vs. 1.46±0.34, 1.76±0.51; infiltratedcells (×105/mL): 2.05±0.48 vs. 0.40±0.08, 0.60±0.23; IL-1β (ng/L): 119.82±6.56 vs. 76.15±3.32, 79.39±4.44; IL-6 (μg/L): 4.10±0.52 vs. 1.97±0.40, 2.27±0.36; TNF-α (mg/L): 1.49±0.28 vs. 0.43±0.23, 0.61±0.24; all P < 0.05], IL-1β, IL-6 and TNF-α levels in serum were also elevated [IL-1β (ng/L): 127.53±7.10 vs. 79.40±2.80, 82.95±2.25; IL-6 (μg/L): 6.28±0.82 vs. 2.96±0.35, 3.36±0.72; TNF-α (mg/L): 1.59±0.42 vs. 0.53±0.22, 0.78±0.25; allP < 0.05]. The mRNA expressions and protein levels of LC3B, COX-Ⅳ and NF-κB p65 in lung tissue of HVT group were significantly higher than those of CON group and NVT group, the mRNA expressions of LC3B-Ⅱ, COX-Ⅳ and NF-κB p65 were (3.52±0.90), (3.76±1.16) and (9.54±2.06) folds of those in CON group, and the protein expressions were (1.76±0.24), (1.65±0.20) and (1.91±0.12) folds of those in CON group, with significantly statistical differences (allP < 0.05). There were no significant differences in the parameters mentioned above between NVT group and CON group.Conclusion Mitophagy may be associated with VILI resulting from escaped mitochondrial DNA for activation of inflammation.

ObjectiveTo investigate the role and its mechanism of the NOD-like receptor 3 (NLRP3) inflammasome in alveolar macrophages in ventilator-induced lung injury (VILI) in rats.Methods Thirty adult male Sprague-Dawley (SD) rats were randomly divided into three groups, with 10 rats in each group: spontaneous breathing control group, normal tidal volume (VT) group (VT 8 mL/kg) and high VT group (VT 40 mL/kg). All of the rats underwent tracheotomy. Then rats in spontaneous breathing control group were kept to have spontaneous breathing, while rats in normal VT group and high VT group received mechanical ventilation. After 4 hours, the rats were sacrificed by carotid artery bleeding, and the bronchoalveolar lavage fluid (BALF), blood serum and lung tissue were collected. Lung wet/dry ratios (W/D) were measured. Light microscopy and electron microscopy were performed to observe the pathological changes in lung tissue, and the ultrastructural changes in alveolar macrophages. Enzyme linked immunosorbent assay (ELISA) was performed to measure the total protein content in the BALF and the interleukins (IL-1β and IL-18) in the serum and BALF. The mRNA expressions and protein levels of NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), caspase-1, and nuclear factor-κB (NF-κB) in alveolar macrophages were assayed by real-time fluorescent quantization reverse transcription-polymerase chain reaction (RT-PCR) and Western Blot.Results The structure of lung tissue and alveolar macrophages of rats in spontaneous breathing control group and normal VT group appeared normal, while obvious inflammatory changes were found in high VT group. Compared with spontaneous breathing control group and normal VT group, the ratio of W/D (8.89±0.90 vs. 5.18±0.86, 5.71±0.82, bothP< 0.05), contents of total protein, IL-1β, IL-18 in BALF were significantly increased [total protein (g/L):2.34±0.41 vs. 1.77±0.14, 1.81±0.06, IL-1β (ng/L): 133.48±10.48 vs. 81.54±3.12, 83.80±5.22, IL-18 (μg/L):4.57±0.45 vs. 3.04±0.51, 3.43±0.43, allP< 0.05], and IL-1β and IL-18 in serum were also increased [IL-1β(ng/L): 105.06±10.18 vs. 65.11±8.58, 75.30±10.62, IL-18 (μg/L): 2.27±0.09 vs. 1.18±0.34, 1.43±0.15, all P< 0.05]. The mRNA and protein expressions of NLRP3, ASC, caspase-1 and NF-κB in alveolar macrophages of high VT group were significantly increased compared with that of spontaneous breathing control group and normal VT group. The mRNA expressions of NLRP3, ASC, caspase-1 and NF-κB in high VT group were (8.53±2.21), (5.75±1.17), (7.47±1.23) and (10.86±2.38) folds of those in spontaneous breathing control group, and the protein expressions of NLRP3, ASC, caspase-1 and NF-κB were (1.50±0.14), (1.49±0.04), (1.53±0.15) and (1.51±0.11) folds of those in spontaneous breathing control group (allP< 0.01). There were no significant differences in all the indexes between normal VT group and spontaneous breathing control group.ConclusionNLRP3 inflammasome in alveolar macrophages may be involved in the mechanism of occurrence of VILI.

Objective To explore the effects of penehyclidine hydrochloride (PHC) on lung epithelial type Ⅱcells against oxidative stress damage. Methods A549 cells treated with H2O2 were used as oxidative stress damage cell model. A549 cells were divided into 3 groups: control group (C group), H2O2 treated group (H group) and PHC treated group (P group). The viability of A549 cells was measured by MTT assay. The apoptotic rate was measured by TUNEL assay. The lev?els of malonicdialed (MDA), reactive oxygen species (SOD), reduced glutathione hormone (GSH) and nicotinamide adenine dinucleotide phosphate (NADPH) of cells were detected by biochemistry colorimetry. Results Compared with group C, the viability of A549 and the contents of SOD, GSH and NADPH were significantly decreased in group H, while MDA content and apoptotic rate were increased (P<0.05). Compared with group H, the viability of A549, the contents of SOD, GSH and NADPH were significantly increased in group P, while MDA content and apoptotic rate were reduced (P<0.05). Conclu?sion Penehyclidine hydrochloride shows protective effects on A549 cells through reducing the oxidative damage induced by H2O2.

Objective To investigate the role of Ras-related C3 botulinum toxin substrate 1/mitogen-activated protein kinase/extracellular signal-regulated kinase (Rac 1/MAPK/ERK) signal pathway in rats with ventilator induced lung injury (VILI) and its mechanism.Methods Thirty Sprague-Dawley (SD) rats were randomly divided into spontaneous respiration group,normal tidal volume (VT) group and high VT group with 10 rats in each group.The rats in spontaneous respiration group were kept their spontaneous breathing.The rats in normal VT group and high VT group were performed tracheal intubation after tracheostomy,and underwent mechanical ventilation on bilateral lungs with 6 mL/kg and 40 mL/kg VT respectively with maintenance anesthesia.After 4-hour ventilation,heart blood,bronchoalveolar lavage fluid (BALF) and lung tissues were harvested.The levels of interleukins (IL-1β,IL-6),tumor necrosis factor-α (TNF-α),myeloperoxidase (MPO) and macrophage inflammatory protein-2 (MIP-2) in serum and BALF were determined by enzyme linked immunosorbent assay (ELISA).Lung wet/dry radio (W/D) was determined.The lung tissues were stained with hematoxylin and eosin (HE),and pathological changes were observed,and pathological scores were evaluated.The ultra structure changes in type Ⅱ alveolar epithelial cells (AEC Ⅱ)were observed with transmission electron microscope.The positive expressions of phosphorylation of extracellular signal-regulated kinase (p-ERK) were determined by immunohistochemistry,and those of Racl and F-actin were determined by immunofluorescence.The mRNA expressions of ERK and Rac1 were determined by real-time fluorescent quantitation reverse transcription-polymerase chain reaction (RT-qPCR),and protein expressions of Rac-1,p-ERK and F-actin were determined by Western Blot.Results ① Compared with spontaneous breathing group,lung W/D in both mechanical ventilation groups was significantly increased,with more significant increase in the high VT group (6.64 ± 0.88 vs.1.79 ± 0.36,P ＜ 0.01).② There was no obvious pathological changes in the lung tissue and AEC Ⅱ of the spontaneously breathing group.In the normal VT group,there was slight edema and infiltration of inflammatory cells;AEC Ⅱ had less lamellar bodies and uniform distribution of the villi of the alveolar epithelium.In the high VT group,the edema of the lung tissue,the widening of the pulmonary septum,the alveolus congestion,the infiltration of inflammatory cells,and alveolar structure disorder were found;and AEC Ⅱ was irregular,the number of lamellar bodies in the plastids was decreased and was unevenly distributed.The pulmonary histopathological score in the high VT group was significantly higher than that in the spontaneous breathing group and the normal VT group (12.00 ± 2.00 vs.6.00 ± 1.51,8.50 ± 0.53,both P ＜ 0.01).③ Compared with spontaneous breathing group,IL-1β,IL-6,TNF-α,MPO,and MIP-2in serum and BALF in both mechanical ventilation groups were significantly increased,with more siguificant increase in the high VT group [serum IL-1 β (ng/L):104.2 ± 15.1 vs.20.3 ± 8.3,IL-6 (ng/L):46.6 ± 11.5 vs.22.7 ± 7.5,TNF-α (ng/L):39.4±6.5 vs.5.4± 1.9,MPO (ng/L):0.66±0.24 vs.0.06±0.03,MIP-2 (ng/L):109.2±25.8 vs.22.8±8.4;BALF IL-1 β (ng/L):121.5 ± 25.6 vs.24.0 ± 7.5,IL-6 (ng/L):136.7 ± 32.7 vs.31.4 ± 10.5,TNF-α (ng/L):98.0 ± 14.8vs.10.1 ±2.6,MPO (ng/L):0.80±0.31 vs.0.08±0.04,MIP-2 (ng/L):144.4±28.9 vs.41.2±20.7;all P ＜ 0.01].④ There were only a few p-ERK,Rac1 and F-actin positive expressions in the spontaneous breathing group.The positive expressions in normal VT group were increased.In high VT group,the positive expression of p-ERK was significantly increased;Rac1 and F-actin were mainly distributed in the cell membrane and cytoplasm respectively,the positive expressions were further enhanced.⑤ The gene expressions of ERK and Rac1,and protein expressions of p-ERK,Rac1 and F-actin in the high VT group were significantly higher than those in the spontaneous breathing group and normal VT group [ERK mRNA (2-△△Ct):8.23±2.83 vs.1,3.02± 1.38,p-ERK protein (gray value):1.15±0.36 vs.0.61 ±0.23,0.88±0.22;Rac1 mRNA (2-△△Ct):4.45 ±2.26 vs.1,1.22±0.39,Rac1 protein (gray value):0.91 ±0.16 vs.0.48±0.11,0.55 ± 0.10;F-actin protein (gray value):0.70± 0.09 vs.0.49 ± 0.08,0.55 ± 0.04;all P ＜ 0.01].Conclusion F-actin expression in lung tissue was up-regulated in rats with VILI,which resulted in reconstruction of AEC Ⅱ cyto-skeleton,and variation of cell membrane permeability through Rac 1 /MAPK/ERK sigualing pathway during VILI.

Objective To evaluate the role of Toll-like receptor 2/nuclear factor-κB(TLR2/NF-κB)signaling pathway pretreatment in ventilator-induced lung injury(VILI). Methods Thirty male Sprague-Dawley(SD)rats were randomly divided into three groups by using random number scale,with 10 rats in each group. Group A:rats were given 200μL of TLR2 monoclonal antibodies(TLR2mAb,10μg/kg)by slow instillation through tracheal catheter, and then ventilated with a high tidal volume(VT)of 40 mL/kg. Group B:ventilated with a normal VT of 8 mL/kg. Group C:rats were tracheally instilled with 10 μg/kg of TLR2mAb devoid of biologic activity,and then ventilated with a high VT of 40 mL/kg. The rats were mechanically ventilated for 4 hours,the lung wet to dry weight ratio(W/D)was calculated. The changes in pathology and ultrastructure in lung tissue were observed with microscope. Enzyme linked immunosorbent assay(ELISA)was performed to determine the concentration of interleukins(IL-1β,IL-6)and tumor necrosis factor-α(TNF-α)in serum and brconchoalveolar lavage fluid(BALF). Real-time fluorescent quantitation reverse transcription-polymerase chain reaction(RT-PCR)was used to assess the mRNA expressions of TLR2, NF-κB and myeloid differentiation factor 88(MyD88)in lung tissue. Results No obvious pathological changes in lungs were found in group A and group B,and no obvious damages to ultra-microstructure were found in lung macrophages, typeⅠepithelial cell and typeⅡepithelial cell. In group C,pathological changes were observed,including pulmonary alveoli fusion,alveoli septum thickening,inflammatory cells infiltration,and damages to ultrastructure of lung macrophage,damage to cell membrane of typeⅠepithelial cells and typeⅡepithelial cells,vacuoles in cytoplasm, damage to organelle,and even pyknosis and perinuclear cistern thickening. Compared with group C,W/D ratio and mean concentration of inflammatory cytokines in serum and BALF showed a significant decrease in group A and B〔W/D ratio:1.151±0.026,1.128±0.048 vs. 1.403±0.062;concentration of IL-1βin serum(ng/L):37.05±5.61, 34.52±4.31 vs. 51.45±8.18;concentration of IL-6 in serum(ng/L):53.65±5.16,55.77±5.62 vs. 89.96±7.08;concentration of TNF-αin serum(ng/L):71.93±13.29,67.36±11.42 vs. 96.20±11.60;concentration of IL-1βin BALF(ng/L):56.48±6.16,54.44±7.26 vs. 99.77±8.41;concentration of IL-6 in BALF(ng/L):172.44±21.26, 163.47±18.70 vs. 216.22±23.90;concentration of TNF-α in BALF(ng/L):235.81±42.75,231.72±40.38 vs. 374.85±69.61,all P<0.01〕,but there were no significant differences between group A and group B(all P>0.05). The mRNA expressions of TLR2,MyD88,and NF-κB were significantly decreased in group A and group B compared with those in group C〔TLR2 mRNA(2-ΔΔCt):1.021±0.287,0.938±0.196 vs. 3.862±0.871;MyD88 mRNA (2-ΔΔCt):1.235±0.277,1.300±0.306 vs. 3.618±1.107;NF-κB mRNA(2-ΔΔCt):0.519±0.036,1.043±0.170 vs. 20.280±9.466,P<0.05 or P<0.01〕,but there was no significant difference among the parameters mentioned above between group A and B(all P>0.05). Conclusion To some extent,pre-intervention with TLR2mAb to block the TLR2/NF-κB signal pathway can inhibit the release of pro-inflammatory factors,and regulate the VILI.

Objective To evaluate the changes in the expression of aquaporin 1 (AQP1) and aquaporin4 (AQP4) in lung tissues during one-lung ventilation in patients undergoing pulmonary lobectomy.Methods Forty ASA physical status Ⅰ or Ⅱ patients,aged 30-64 yr,weighing 45-79kg,undergoing pulmonary lobectomy,were randomly divided into 2 groups(n=20 each):two-lung ventilation group (group T) and one-lung ventilation group (group O).Anesthesia was induced with iv injection of midazolam,fentanyl,vecuronium and propofol.In group T,the patients were intubated with a single-lumen endotracheal tube and two-lung ventilation was performed.In group O,double-lumen endobranchial tube was inserted,and two-lung ventilation was performed followed by onelung ventilation after chest opening.PET CO2 was maintained at 5.3-24.0 kPa and SpO2 was maintained ＞ 92％.Anesthesia was maintained with iv infusion of remifentanil,propofol and vecuronium.The normal lung tissues were obtained from the site near the pathologic changes for microscopic examination (with light microscope) and examination of the ultrastructure (with transmission electron microscope),and for determination of W/D lung weight ratio,the expression of AQP1 mRNA and AQP4 mRNA (by RT-PCR) and the expression of AQP1 protein and AQP4 protein (by Western blot).Results Compared with group T,W/D lung weight ratio was significantly increased,the expression of AQP1 mRNA and protein was down-regulated in group O (P ＜ 0.05),and no significant changes were found in the expression of AQP4 mRNA and protein in group O (P ＞ 0.05).Pathological changes were observed in group O.Conclusion Down-regulation of AQP1 expression may be involved in the acute lung injury induced by one-lung ventilation in patients undergoing pulmonary lobectomy,however,AQP4 has no such effect.

Objective To investigate the changes in the expression of macrophage migration inhibitory factor (MIF) mRNA in a rat model of ventilator-induced lung injury.Methods Thirty adult male Sprague-Dawley rats,weighing 2β5-260 g,were randomly divided into 3 groups (n =10 each) using a random number table:control group (group C),small tidal volume (VT) mechanical ventilation group (group S) and large tidal volume mechanical ventilation group (group L).The animals were anesthetized with intraperitoneal ketamine 100 mg/kg,midazolam 0.2 mg/kg and atropine 1.0 mg/kg.The rats were tracheostomized and spontaneous breathing was maintained in group C,while the rats were tracheostomized and mechanically ventilated for 4 h in groups S and L.The tidal volume was 7 ml/kg (group S) or 40 ml/kg (group L),I ∶ E was 1 ∶ 1,RR was 80 bpm and FiO2 was 100％.At 4 h of spontaneous breathing or mechanical ventilation,broncho-alveolar lung lavage fluid (BALF) was collected for determination of the total protein concentration,white blood cell (WBC) counts and concentrations of MIF,IL-6 and IL-1β (by ELISA).Then the rats were sacrificed and the lungs removed for microscopic examination and for determination of wet to dry lung weight ratio (W/D ratio) and expression of MIF mRNA (by RT-PCR).Results Compared with C and S groups,WBC counts,concentrations of total protein,MIF,IL-6 and IL-1β in BALF,and W/D ratio and expression of MIF mRNA in lung tissues were significantly increased in group L (P ＜ 0.05).There was no significant difference in the indexes mentioned above between group C and group S (P ＞ 0.05).The pathological changes occurred in group L.Conclusion The up-regulation of MIF mRNA expression in lung tissues may be involved in the development of ventilator-induced lung injury in rats.

Objective To investigate the role of Toll-like receptor9 (TLR9)-myeloid differentiation factor 88 (MyD88) signal pathway in alveolar macrophages in ventilator-induced lung injury (VILI).Methods 30 adult male Sprague-Dawley (SD) rats were randomly assigned to three groups (with 10 rats in each group).Group A was the control group,with spontaneous respiration after tracheostomy.Rats in group B received mechanical ventilation for 4 hours with normal tidal volume (VT) 7 ml/kg after tracheostomy,and group C rats received mechanical ventilation with VT 40 ml/kg for 4 hours.After termination of ventilation,examination with transmission electron microscopy was performed to observe the ultrastructure changes in alveolar epithelial cell type Ⅱ (AEC Ⅱ) of the lung.Lung wet/dry ratios (W/D) and total protein concentration,the concentration of interleukins (IL-6 and IL-1 β) in bronchoalveolar lavage fluid (BALF) were determined.The protein and mRNA expressions of TLR9,MyD88 and nuclear factor-κB (NF-κB) in alveolar macrophages were assayed by Western Blot and real-time reverse transcription-polymerase chain reaction (RT-PCR).Results The ultrastructure of AEC Ⅱ in the group A and group B was almost normal,whereas the chromatin of the nuclei,the lamellar corpuscles in the cytoplasm,the cell membrane and the microvilli of the AEC Ⅱ in the group C showed injurious changes in various degrees.When the group C was compared with the group A and the group B,it was shown that the W/D ratios (5.54 ± 0.17 vs.4.58 ± 0.17,4.69 ± 0.16) and total protein concentration (g/L:6.33 ± 0.61 vs.0.45 ± 0.05,0.47 ± 0.04),IL-6 (μg/L:1.989 ± 0.103 vs.1.033 ± 0.061,1.010 ± 0.069) and IL-lβ (ng/L:2.79 ±0.25 vs.1.05 ±0.15,1.23 ±0.22) in BALF,the protein expressions of TLR9,MyD88 and NF-κB [TLR9 (A value):0.770 ±0.042 vs.0.300 ±0.027,0.310 ±0.037; MyD88 (A value):0.950 ±0.091 vs.0.560 ±0.082,0.580±0.084; NF-κB(A value):1.020 ±0.076 vs.0.740 ±0.052,0.700 ±0.076] in alveolar macrophages were all increased significantly,and all of which showed significant difference (P＜0.05 or P＜0.01).The mRNA levels of TLR9,MyD88 and NF-κB in alveolar macrophages in the group B were (1.13 ± 0.32),(1.18 ± 0.33),and (1.11 ± 0.22) folds of those of the group A,respectively,but there were no significant differences (all P＞0.05).While the mRNA levels of TLR9,MyD88 and NF-κB of alveolar macrophages in the group C were (8.66 ± 0.69),(6.41 ± 0.53) and (5.29 ± 0.71) folds of those of the group A,respectively,and all of them showed significant difference (all P＜0.01).Conclusion TLR9-MyD88 signaling in alveolar macrophages plays a role in pathogenesis of VILI.

Objective To evaluate the association between recurrent miscarriages and insulin resistance.Methods The case-control studies on the association between recurrent spontaneous abortion and insulin resistance from June 1996 to April 2012 were collected from Medline,Elsevier,Chinese Journal Fulltext Database,Chinese Biological Medicine Database,data base of Wanfang,Springer link and EMBASE.RevMan 5.1 software was used for Meta analysis.Results According to the included criteria,7 clinical trials were finally selected.Total 467 cases with recurrent pregnancy loss were enrolled in study group,while 413 women with no history of abnormal pregnancies were enrolled in control group.No significant difference was found in average age and body mass index between the two groups (P ＞ 0.05).Meta analysis results showed that the level of fasting glucose was no statistical difference between study group and control group (WMD =2.27,95％ CI:-1.11 to 5.65,P ＞0.05); fasting insulin level was higher 2.05 mU/L in study group than that of in control group,the difference was statistically significant (WMD =2.05,95％ CI:1.03 to 3.08,P ＜ 0.01).Case number of study group on Homa-insulin resistance ＞ 4.5 was more than that of control group (OR =3.36,95％ CI:1.72 to 6.57,P ＜ 0.01).Case number of study group on glucose/insulin ratio ＜ 4.5 was more than that of the control group,statistical difference was found (OR =3.37,95％ CI:1.90 to 5.99,P ＜ 0.01).Conclusion Insulin resistance is associated with the susceptibility to recurrent miscarriages,and it may contribute to the occurrence of recurrent miscarriages.

Objective:To detect the value of utilizing bpMRI in prostate biopsy in the detection of prostate cancer with PSA≤20ng/ml.Methods:The clinical data of 394 patients who underwent prostate biopsy in the First Affiliated Hospital of Nanjing Medical University from November 2017 to October 2019 were retrospectively analyzed. Of all the patients, 177 underwent modified systematic biopsy, named TRUS group, 217 patients accepted pre-biopsy bpMRI examination, undergoing modified systematic biopsy if Prostate Imaging Reporting and Data System (PI-RADS) score < 3 or MRI-TRUS cognitive fusion targeted prostate + systematic biopsy if PI-RADS score ≥ 3, named MRI group. The median age of TRUS group was 66 (61, 74) years old, prostate specific antigen (PSA) was 9.52 (7.26, 12.30) ng / ml, and prostate volume (PV) was 36.84 (28.95, 57.72)ml. The median age of MRI group was 66 (59, 72) years old, PSA was 8.84 (6.65, 12.16) ng/ml, and PV was 39.45 (29.25, 58.69)ml. There was no difference in above parameters between the two groups. The χ 2 test was used to compare the detection rate of prostate cancer and clinically significant prostate cancer (CsPCa) between the two groups. Results:There was no significant difference in the detection rates of prostate cancer between TRUS group and MRI group [51.41% (91/177) vs. 48.39% (105/ 217), P = 0.550], but the detection rates of CsPCa were significantly different [26.55% (47/177) vs. 36.41% (79/217), P = 0.037]. In patients with PSA ≤ 10 ng / ml, there was no significant difference in the detection rates of prostate cancer between the two groups [43.62% (41/94) vs. 43.08% (56/130), P = 0.936], but there was a significant difference in the detection rates of CsPCa [17.02% (16/94) vs. 28.46% (37/130), P = 0.047]. There was no significant difference in the detection rates of prostate cancer [60.24% (50/83) and 56.17% (48/87), P= 0.504] and the detection rates of CsPCa [37.35% (31/83) vs. 48.28% (42/87), P = 0.150] between the two groups. The total detection rates of the last two needles in TRUS group and MRI group were 23.16% (41/177) and 36.63% (86/217), respectively, with significant difference ( P=0.001); the detection rates of CsPCa in the last two needles were 11.86% (26/177) and 29.03% (63/ 217), respectively, with significant difference ( P < 0.001). In MRI group, the detection rates of prostate cancer in patients with PI-RADS score <3, 3, 4, 5 were 21.21% (7/33), 25.84% (23/89), 73.24% (52/71), 95.83% (23/24), respectively; the detection rates of CsPCa were 12.12% (4/33), 17.98% (16/89), 54.93% (39/71), 83.33% (23/24), respectively. Conclusions:In patients with PSA ≤ 20 ng / ml, prostate biopsy based on bpMRI may improve the detection of CsPCa, especially in patients with PSA ≤ 10 ng/ml.