1.Exploring mechanism of TLR4/NF-κB-NLRP3 inflammasome signaling pathway in experimental autoim-mune prostatitis rats
Liangxi LU ; Hong SHI ; Zhimin HUANG ; Jie LU ; Wenjie WANG
The Journal of Practical Medicine 2025;41(6):800-805
Objective The pathogenesis of EAP in rats based on the TLR4/NF-κB-NLRP3 inflammasome signaling pathway was explored.Methods Randomly divide 12 male SD rats into 4 groups using the number table,namely normal group(N),model group(M),Caspase-1 inhibitor group(Caspase-1),and NLRP3 inhibitor MCC950 group(NLRP3),with 3 rats in each group.After drug intervention,relevant indicators were observed by using HE staining,ELISA,WB methods.Results Compared with the N group,the M group rats had showed significant damage in prostate gland structure and infiltration of inflammatory cells.Compared with group N,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the prostate tissue of group M rats had increased(P<0.01).Compared with group M,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the NLRP3 and Caspase-1 groups had significantly reduced(P<0.01).The serum levels of IL-1 β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-α in group M rats had been significantly higher than those in group N(P<0.01).But the serum levels of IL-10 had been slightly lower and no statistical significance.The serum levels of IL-1β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-α in group M rats had been lower than those in group N(P<0.01 or P<0.05),the serum IL-10 level had increased(P<0.01).Conclusion The activation of TLR4/NF-κB-NLRP3 inflammasome signaling path-way promotes the occurrence and development of prostatitis in EAP rats.
2.MiRNA-155-5p aggravates renal injury in lupus nephritis by targeting OCS1 to regulate the JAK2/STAT3 signaling pathway
Aitao LIN ; Zhimin HUANG ; Zhiying ZHANG ; Tingna FU ; Liangxi LU ; Xiaoyu LIU ; Yini JIANG ; Leilei ZHAO ; Jinyu WU
The Journal of Practical Medicine 2025;41(9):1285-1292
Objective To investigate the effect and mechanism of miR-155-5p targeting suppressor of cytokine signaling 1(SOCS1)in regulating the Janus kinase 2(JAK2)/signal transducer and activator of transcrip-tion 3(STAT3)signaling pathway in renal injury associated with lupus nephritis(LN).Methods Thirty female MRL-faslpr lupus model mice were randomly divided into five groups(n=6 per group):the model group,the antagomir NC group,the miR-155-5p antagomir group,the miR-155-5p antagomir+shRNA control group,and the miR-155-5p antagomir+SOCS1 shRNA group.The mice were treated with adeno-associated virus vectors carrying miR-155-5p antagomir,antagomir NC,SOCS1 shRNA,or shRNA control.Additionally,six age-matched C57BL/6 mice served as a control group and received an equivalent volume of saline.Serum blood urea nitrogen(BUN)and creatinine(Scr)levels,renal histopathological changes,and the expression levels of miR-155-5p,SOCS1,phosphorylated JAK2(p-JAK2),and phosphorylated STAT3(p-STAT3)in renal tissues were evaluated.Results Compared with the normal group,the model group exhibited significantly elevated levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins in the kidneys(P<0.01),while the expression level of SOCS1 was markedly reduced(P<0.01).Compared with both the model group and the antagomir NC group,the miR-155-5p antagomir group showed decreased levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),along with a significant increase in SOCS1 expression(P<0.01).Similarly,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group demon-strated significantly higher levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),while SOCS1 expression was notably decreased(P<0.01).Renal pathology analysis revealed that,compared to the normal group,the model group exhibited glomerular atrophy,extensive infiltration of inflammatory cells in the renal tubulointerstitial region,and partial renal tubular necrosis.In contrast,the miR-155-5p antagomir group showed marked improvements in glomerular atrophy,tubular necrosis,and inflammatory cell infiltration compared with the model group and antagomir NC group.Furthermore,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group exhibited more severe glomerular atrophy,tubular necrosis,and inflammatory cell infiltration.Conclusion MiR-155-5p exacerbates renal damage in MRL-faslpr lupus model mice by targeting SOCS1,potentially through the activation of the JAK2/STAT3 signaling pathway.
3.To investigate the mechanism of mitochondrial autophagy regulating the expression of NLRP3 inflamma-some in prostate tissue in rats with experimental autoimmune prostatitis
Liangxi LU ; Haiwang LU ; Wenjie WANG ; Jun SHI ; Zhimin HUANG ; Bin BIN
The Journal of Practical Medicine 2025;41(12):1816-1824
Objective To investigate the mechanism of mitochondrial autophagy regulating the expression of NLRP3 inflammasome in prostate tissue in experimental autoimmune prostatitis(EAP)rats and to provide a theoretical basis for the study of new drug development.Methods A numerical table of 40 SD male rats was randomly divided into 8 groups.Namely,normal group(N),model group(M),rapamycin group(RAP),rapamycin+mitochondrial autophagy inhibitor group(RAP+Mdivi-1),autophagy inhibitor group(3MA),mitochondrial autophagy inhibitor group(Mdivi-1),Caspase1 inhibitor group(Caspase1),NLRP3 inhibitor group(NLRP3),5 animals per group.After drug intervention,HE staining,immunofluorescence,colorimetry,and WB method were used to observe the relevant indexes.Results Compared with group N,the structural damage of prostate gland was obvious in group M.Compared with the M group,the prostate gland structure in RAP group,Caspase-1 group and NLRP3 group were improved.However,that in 3-MA group and Mdivi-1 group was not improved,and even destroyed more obvi-ously.Compared with group N,the co-expression of LC3-II and LAMP-1 was enhanced,mitochondrial membrane potential was decreased,ROS release level was significantly increased in prostate tissue of rats in group M.Com-pared with the M group,the above indexes in RAP group and NLRP3 group were significantly improved.However,the above indexes in 3-MA group and Mdivi-1 group became worse.Compared with group N,the protein expressions of DRP1,PINK1 and Parkin in prostate mitochondria of rats in group M were increased,and the protein expres-sions of OPA1 was decreased.Compared with group M,the protein expressions of DRP1,PINK1 and Parkin in RAP group and NLRP3 group were significantly increased,while those in 3-MA group and Mdivi-1 group were sig-nificantly decreased.OPA1 protein expression was significantly decreased in the RAP group.The protein expression of Parkin in Caspase-1 group was decreased,but the protein expression of DRP1,OPA1 and PINK1 had no significant difference.Compared with group N,the protein expressions of LC3II/LC3I,Beclin1,NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β,and IL-18 in prostate tissue of rats in group M were increased,while the protein expres-sions of P62 was decreased.Compared with M group,LC3II/LC3I and Beclin1 protein expressions in RAP group and NLRP3 group were significantly increased,while those in 3-MA group and Mdivi-1 group were significantly decreased.Compared with M group,P62,NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β and IL-18 protein expressions in RAP group and NLRP3 group were significantly decreased,while those in 3-MA group and Mdivi-1 group were significantly increased.Compared with M group,the protein expressions of NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β,and IL-18 in Caspase-1 group were significantly reduced,but the protein expressions of LC3Ⅱ/LC3Ⅰ,Beclin1,and P62 were not statistically significant.Conclusions NLRP3 inflammatosome is involved in the progression of chronic prostatitis in EAP rats.Mitochondrial autophagy mediates the occurrence and development of prostatitis in EAP by regulating the activation of NLRP3 inflammasome in prostate tissue.
4.Exploring mechanism of TLR4/NF-κB-NLRP3 inflammasome signaling pathway in experimental autoim-mune prostatitis rats
Liangxi LU ; Hong SHI ; Zhimin HUANG ; Jie LU ; Wenjie WANG
The Journal of Practical Medicine 2025;41(6):800-805
Objective The pathogenesis of EAP in rats based on the TLR4/NF-κB-NLRP3 inflammasome signaling pathway was explored.Methods Randomly divide 12 male SD rats into 4 groups using the number table,namely normal group(N),model group(M),Caspase-1 inhibitor group(Caspase-1),and NLRP3 inhibitor MCC950 group(NLRP3),with 3 rats in each group.After drug intervention,relevant indicators were observed by using HE staining,ELISA,WB methods.Results Compared with the N group,the M group rats had showed significant damage in prostate gland structure and infiltration of inflammatory cells.Compared with group N,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the prostate tissue of group M rats had increased(P<0.01).Compared with group M,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the NLRP3 and Caspase-1 groups had significantly reduced(P<0.01).The serum levels of IL-1 β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-α in group M rats had been significantly higher than those in group N(P<0.01).But the serum levels of IL-10 had been slightly lower and no statistical significance.The serum levels of IL-1β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-α in group M rats had been lower than those in group N(P<0.01 or P<0.05),the serum IL-10 level had increased(P<0.01).Conclusion The activation of TLR4/NF-κB-NLRP3 inflammasome signaling path-way promotes the occurrence and development of prostatitis in EAP rats.
5.To investigate the mechanism of mitochondrial autophagy regulating the expression of NLRP3 inflamma-some in prostate tissue in rats with experimental autoimmune prostatitis
Liangxi LU ; Haiwang LU ; Wenjie WANG ; Jun SHI ; Zhimin HUANG ; Bin BIN
The Journal of Practical Medicine 2025;41(12):1816-1824
Objective To investigate the mechanism of mitochondrial autophagy regulating the expression of NLRP3 inflammasome in prostate tissue in experimental autoimmune prostatitis(EAP)rats and to provide a theoretical basis for the study of new drug development.Methods A numerical table of 40 SD male rats was randomly divided into 8 groups.Namely,normal group(N),model group(M),rapamycin group(RAP),rapamycin+mitochondrial autophagy inhibitor group(RAP+Mdivi-1),autophagy inhibitor group(3MA),mitochondrial autophagy inhibitor group(Mdivi-1),Caspase1 inhibitor group(Caspase1),NLRP3 inhibitor group(NLRP3),5 animals per group.After drug intervention,HE staining,immunofluorescence,colorimetry,and WB method were used to observe the relevant indexes.Results Compared with group N,the structural damage of prostate gland was obvious in group M.Compared with the M group,the prostate gland structure in RAP group,Caspase-1 group and NLRP3 group were improved.However,that in 3-MA group and Mdivi-1 group was not improved,and even destroyed more obvi-ously.Compared with group N,the co-expression of LC3-II and LAMP-1 was enhanced,mitochondrial membrane potential was decreased,ROS release level was significantly increased in prostate tissue of rats in group M.Com-pared with the M group,the above indexes in RAP group and NLRP3 group were significantly improved.However,the above indexes in 3-MA group and Mdivi-1 group became worse.Compared with group N,the protein expressions of DRP1,PINK1 and Parkin in prostate mitochondria of rats in group M were increased,and the protein expres-sions of OPA1 was decreased.Compared with group M,the protein expressions of DRP1,PINK1 and Parkin in RAP group and NLRP3 group were significantly increased,while those in 3-MA group and Mdivi-1 group were sig-nificantly decreased.OPA1 protein expression was significantly decreased in the RAP group.The protein expression of Parkin in Caspase-1 group was decreased,but the protein expression of DRP1,OPA1 and PINK1 had no significant difference.Compared with group N,the protein expressions of LC3II/LC3I,Beclin1,NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β,and IL-18 in prostate tissue of rats in group M were increased,while the protein expres-sions of P62 was decreased.Compared with M group,LC3II/LC3I and Beclin1 protein expressions in RAP group and NLRP3 group were significantly increased,while those in 3-MA group and Mdivi-1 group were significantly decreased.Compared with M group,P62,NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β and IL-18 protein expressions in RAP group and NLRP3 group were significantly decreased,while those in 3-MA group and Mdivi-1 group were significantly increased.Compared with M group,the protein expressions of NLRP3,ASC,Cleaced-Caspase1,Cleaced-IL-1β,and IL-18 in Caspase-1 group were significantly reduced,but the protein expressions of LC3Ⅱ/LC3Ⅰ,Beclin1,and P62 were not statistically significant.Conclusions NLRP3 inflammatosome is involved in the progression of chronic prostatitis in EAP rats.Mitochondrial autophagy mediates the occurrence and development of prostatitis in EAP by regulating the activation of NLRP3 inflammasome in prostate tissue.
6.MiRNA-155-5p aggravates renal injury in lupus nephritis by targeting OCS1 to regulate the JAK2/STAT3 signaling pathway
Aitao LIN ; Zhimin HUANG ; Zhiying ZHANG ; Tingna FU ; Liangxi LU ; Xiaoyu LIU ; Yini JIANG ; Leilei ZHAO ; Jinyu WU
The Journal of Practical Medicine 2025;41(9):1285-1292
Objective To investigate the effect and mechanism of miR-155-5p targeting suppressor of cytokine signaling 1(SOCS1)in regulating the Janus kinase 2(JAK2)/signal transducer and activator of transcrip-tion 3(STAT3)signaling pathway in renal injury associated with lupus nephritis(LN).Methods Thirty female MRL-faslpr lupus model mice were randomly divided into five groups(n=6 per group):the model group,the antagomir NC group,the miR-155-5p antagomir group,the miR-155-5p antagomir+shRNA control group,and the miR-155-5p antagomir+SOCS1 shRNA group.The mice were treated with adeno-associated virus vectors carrying miR-155-5p antagomir,antagomir NC,SOCS1 shRNA,or shRNA control.Additionally,six age-matched C57BL/6 mice served as a control group and received an equivalent volume of saline.Serum blood urea nitrogen(BUN)and creatinine(Scr)levels,renal histopathological changes,and the expression levels of miR-155-5p,SOCS1,phosphorylated JAK2(p-JAK2),and phosphorylated STAT3(p-STAT3)in renal tissues were evaluated.Results Compared with the normal group,the model group exhibited significantly elevated levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins in the kidneys(P<0.01),while the expression level of SOCS1 was markedly reduced(P<0.01).Compared with both the model group and the antagomir NC group,the miR-155-5p antagomir group showed decreased levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),along with a significant increase in SOCS1 expression(P<0.01).Similarly,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group demon-strated significantly higher levels of BUN,Scr,miR-155-5p,p-JAK2,and p-STAT3 proteins(P<0.01),while SOCS1 expression was notably decreased(P<0.01).Renal pathology analysis revealed that,compared to the normal group,the model group exhibited glomerular atrophy,extensive infiltration of inflammatory cells in the renal tubulointerstitial region,and partial renal tubular necrosis.In contrast,the miR-155-5p antagomir group showed marked improvements in glomerular atrophy,tubular necrosis,and inflammatory cell infiltration compared with the model group and antagomir NC group.Furthermore,compared with the miR-155-5p antagomir group and the miR-155-5p antagomir+shRNA control group,the miR-155-5p antagomir+SOCS1 shRNA group exhibited more severe glomerular atrophy,tubular necrosis,and inflammatory cell infiltration.Conclusion MiR-155-5p exacerbates renal damage in MRL-faslpr lupus model mice by targeting SOCS1,potentially through the activation of the JAK2/STAT3 signaling pathway.
7.Effects of Sanqi on Sortilin,TLRs and vascular calcification in rats with chronic renal failure
Zhimin HUANG ; Liangxi LU ; Yini JIANG ; Xiaoyu LIU ; Zhiying ZHANG ; Jinyu WU
The Journal of Practical Medicine 2024;40(6):773-779
Objective Taking Sortilin as the entry point,this study aims to explore the mechanism of vascular calcification in chronic renal failure(CRF)and explore the influence of Sanqi on Sortilin,TLRs and vascular calcification,and to provide an effective method for clinical reduction of cardiovascular events in CRF.Methods Thirty-six male SD rats were randomly divided into normal group,model group,low-,medium-and high-dose Sanqi group and calcitriol group,with 6 rats in each.The replicative CRF vascular calcification rat model was fed with adenine combined with high phosphorus diet.Aortic calcium salt deposition,serum creatinine(Scr),urea nitrogen(BUN),blood calcium(Ca),blood phosphorus(P),total cholesterol(TC),triglyceride(TG),TLRs and Sortilin protein in aorta and inflammatory factors were detected.Results In the model group,renal fibrosis was obvious and many adenine crystals were found in renal interstitium.Large deposits of calcium salts were found.Renal fibrosis and calcium salt deposition were alleviated in different degrees in all treatment groups.Compared with those in the normal group,the level of BUN,Cr,P,TG,TC,IFN-γ,IL-6,IL-10 and IL-17A in the serum of the model group was ascended(P<0.01),while the level of Ca was descended(P<0.01).Compared with those in the model group,the level of BUN,Cr,P,TG,TC,IFN-γ,IL-6,IL-10 and IL-17A in the serum of rats in the Sanqi medium and high dose group and calcitriol group was significantly decreased(P<0.01),and the contents of Ca were significantly increased(P<0.05 or P<0.01).Compared with those in the normal group,the protein expression of BMP2,RUNX2,Sortilin,TLR7 and TLR9 in aortic tissue of rats in the model group was elevated(P<0.01),while the protein expression of SM22α was declined(P<0.01).Compared with those in the model group,the protein expression of BMP2,RUNX2,Sortilin,TLR7,and TLR9 in the low-,medium-,and high-dose Sanqi group and calcitriol group was decreased significantly(P<0.01);the protein expression of SM22α was increased significantly(P<0.05 or P<0.01),and the high-dose Sanqi group and calcitriol group had more significant effects.Conclusion Sanqi can improve renal fibrosis and vascular calcification in CRF model rats,and its mechanism may be related to the regulation of biological functions of Sortilin and TLRs.
8. Multicenter epidemiological investigation of hospitalized elderly, young and middle-aged patients with severe burn
Yong TANG ; Liangxi WANG ; Weiguo XIE ; Chuan′an SHEN ; Guanghua GUO ; Junjie CHEN ; Chunmao HAN ; Licheng REN ; Zhigang CHU ; Meifang YIN ; Yuan WANG ; Dongxia ZHANG ; Yuesheng HUANG ; Jiaping ZHANG
Chinese Journal of Burns 2017;33(9):537-544
Objective:
To compare and analyze the epidemiological characteristics of hospitalized elderly, young and middle-aged patients with severe burn in recent years, so as to provide reference for the prevention and treatment of elderly patients with severe burn.
Methods:
Relying on the entry system of epidemiological case data and biological sample of severe burn from multicenter in clinic, medical records of patients with severe burn, aged above 18, hospitalized in 8 burn wards from January 2012 to December 2015 were collected. Six hundred and fifteen patients who were more than 18 years old and less than or equal to 65 years old were included in young and middle-aged group (YM). Eighty-two patients aged more than 65 years old were included in elderly group (E). Data of age, gender, residence, education level, cause of injury, location of injury, season of injury, total burn area, occurrence and area of full-thickness burn injury, wound site, inhalation injury incidence and severity, post burn admission time, proportion of delayed resuscitation, proportion of escharectomy or tangential excision and skin grafting, preinjury systemic disease, system complication during hospitalization, length of hospital stay, outcome of treatment, and reason of abandoning treatment of patients were analyzed. Data were processed with chi-square test and Mann-Whitney
9.Application of somatostatin in nonoperative treatment of different kinds of intestinal obstruction
Yanzhang ZHUANG ; Liangxi HUANG ; Peng HUANG
Chinese Journal of Primary Medicine and Pharmacy 2015;22(1):38-41
Objective To investigate the therapeutical effects of somatostatin in nonoperative treatment of different kinds of intestinal obstruction.Methods 338 cases of intestinal obstruction accepted by our hospital were retrospectively analyzed,which were divided into adhesive intestinal obstruction,inflammatory intestinal obstruction and malignant tumor intestinal obstruction.With nonoperative treatment,the control group were treated with routine therapy,including fasting,gastrointestinal decompression,intestinal lavage,intravenous replacement of fluid and electrolytes,disturbance of acid-base balance and the application of antibiotics.As for the treatment group,they were pumped with 6mg of somatostatin and 120mL physiological saline as well as routine therapy for 24 hours.The effects of the two groups were compared.Results The remission rate of abdominal distension and abdominal pains was 80.2% in the treatment group and 62.3% in the control group,the difference was statistical significance (x2 =250.446,P < 0.05).The remission rate of nausea and vomiting was 84.1% in the treatment group and 87.7% in the control group.The passage of gas and defecation by anus was 64.7 % in the treatment group and 61.6% in the control group,there was no clear difference between the two groups (x2 =0.902,0.349,all P > 0.05).The gastrointestinal decompression amounts reduced clearly,the treatment group was (328 ±229) mL/d and (694 ± 381) mL/d in the control group,there was significant difference (t =2.883,P < 0.05).After nonoperative conservative treatment,the effects between the two groups were as follows:the effective percentage was 95.7% in the treatment group and 94.0% in the control group,there was no significant difference(x2 =0.007,P > 0.05).Except intestinal obstruction patients with external tumors,the rates of transferring to operation was 2.4 % in the treatment group and 2.8 % in the control group,there was no statistical significance(x2 =0.051,P > 0.05).And except patients of intestinal obstruction with external tumors and transferring to operation,the hospital stay was (10.6 ±4.9) d in the treatment group and (15.3 ± 4.1) d in the control group,the difference was significant (t =2.528,P < 0.05).As for the treatment group with somatostatin,there was no significant difference(x2 =0.008,0.230,t =0.117,all P > 0.05) in abdominal distension and abdominal pains of adhesive and inflammatory intestinal obstruction,promoting the passage of gas and defecation by anus,the improvement of gastrointestinal decompression amounts in 24 hours.The improvement of tumor intestinal obstruction was worse.Conclusion Somatostatin treatment can help to ease the symptoms and physical signs of different kinds of intestinal obstruction rapidly and cut down hospital stay clearly,but can not reduce the rates of transferring to operation.If the time of treatment is ignored,it can not improve the therapeutical effective percentage of intestinal obstruction obviously.There is no significant difference for the application of adhesive and inflammatory intestinal obstruction.However,it can not completely and well improve the symptoms of tumor intestinal obstruction and the symptoms can recrudesce easily.
10.Evaluation of an optimization method for Eclipse IMRT plan for upper esophageal carcinoma
Jiayang LU ; Lokman CHEUNG ; Baotian HUANG ; Lili WU ; Wenjia XIE ; Liangxi XIE
Chinese Journal of Radiological Medicine and Protection 2015;35(8):584-589
Objective To evaluate the dosimetric characteristics of base dose plan compensation (BDPC) optimization method applied on the intensity-modulated radiotherapy (IMRT) for upper esophageal carcinoma,based on the Eclipse treatment planning system.Methods Nineteen patients were included.For each case initial IMRT plan was generated and further optimized respectively by the two following methods:the BDPC method and hot and cold spot control (HCSC) method.Then the BDPC and HCSC plans were compared concerning planning-target-volume (PTV) coverage,conformity index (CI),and homogeneity index (HI),as well as organ-at-risk (OAR) sparing,planning time,monitor unit (MU) and delivery time.Results Compared with the HCSC plans,the BDPC plans provided superior CI and HI (Z =-3.662,-3.745,P < 0.05),as well as lower D2% (near-maximum dose) (Z =-3.823,P < 0.05) and comparable D98% (near-minimum dose) (P > 0.05) for PTV64 (high-risk PTV),and provided superiorCI (Z=-3.340,P<0.05),lower D95% and D98% (Z=-3.582,-2.616,P<0.05) for PTV54 (low-risk PTV).The BDPC plans also provided slightly lower doses to the spinal cord and lung compared with the HCSC plans (Z =-3.625--3.369,P < 0.05).Moreover,the planning time [(26.05 ±0.88) min] for BDPC plans was less than that of the HCSC plans [(33.73 ± 3.24) min] (Z =-3.823,P <0.05).The MU of the BDPC plans (1 019 ± 167) was higher than that of the HCSC plans (1 003 ±159) (Z=-2.616,P<0.05),while the delivery time [(3.52 ±0.29) min] was more than that of the HCSC plans [(3.50±0.28) min] (Z=-2.548,P<0.05).Conclusions The BDPC optimization method can significantly improve target dose homogeneity and conformity with effective reduction of the dose to OARs for upper esophageal carcinoma.Moreover,it is simple and can improve the treatment planning efficiency.

Result Analysis
Print
Save
E-mail