Objective To investigate the current situation of achievement transformation in tertiary medical hospitals in Shanghai and propose countermeasures for the existing problems to enhance the effectiveness of achievement transformation.Methods A questionnaire survey was done on the transformation and management of scientific research achievements in 47 terti-ary hospitals in Shanghai.Meanwhile,interviews were carried out among the managers and researchers from these hospitals.Re-sults In the past three years,the rate of transformation achievements in the hospitals was only 2.8%.In the achievement trans-formation existed such problems as weak awareness of scientific researchers,low patent quality,lack of full-time managers,and inflexible management mode.It was also believed that there is a need to improve main responsibilities,achievement management,system establishment,personnel training,resource sharing,department coordination and other related aspects.Conclusion The rate of achievement transformation in tertiary medical institutions in Shanghai is at a lower level.There are numerous problems and difficulties in the transformation.Therefore,urgent efficient countermeasures are needed to promote the transformation of a-chievement.

Objective:To investigate the safety and efficacy of balloon pulmonary angioplasty (BPA) for residual pulmonary hypertension (PH) of chronic thromboembolic pulmonary hypertension(CTEPH) after pulmonary endarterectomy (PEA).Methods:Patients diagnosed as PH after PEA in China-Japan Friendship Hospital from Oct 2016 to Jun 2022 were included. The indication for BPA was decided on the basis of a consensus of the multi-disciplinary team for all patients with CTEPH. Before treatment, the patient′s exercise tolerance and pulmonary artery flow parameters were evaluated. A comparative analysis of various parameters before BPA treatment and at the last BPA was conducted. 6-min walk distance (6MWD) was analyzed using the paired Wilcoxon test; N-terminal pro-brain natriuretic peptide (NT-proBNP), mixed venous oxygen saturation, mean pulmonary arterial pressure (mPAP), cardiac index (CI) and pulmonary vascular resistance (PVR) were compared using the paired-samples t-test. WHO functional class was compared using McNemar′s test. Results:Twenty patients with a total of 130 vessels underwent 46 sessions of BPA treatment. The postoperative 6-minute walk distance (6MWD) [447 (415, 485) m] showed a significant improvement compared to the preoperative baseline [389 (335, 470) m] ( Z=6.52, P<0.05), Postoperative mixed venous oxygen saturation (72.0%±1.9%) showed a significant improvement compared to the preoperative levels (64.0%±2.7%) ( t=2.14, P<0.05).Postoperatively, plasma NT-proBNP [(351.9±129.9) pg/ml], mPAP [(24.2±1.9) mmHg], and PVR [(3.0±1.4) WU] significantly decreased compared to preoperative levels [(982.5±426.2) pg/ml, (33±2.1) mmHg, (8.0±1.6) WU)] ( t=3.38, 1.22, 2.10, P<0.05 for all). Postoperatively, there was a significant improvement in WHO functional class (Ⅰ，Ⅱ，Ⅲ，Ⅳ: 14, 4, 2, 0 cases) compared to preoperative status (Ⅰ，Ⅱ，Ⅲ，Ⅳ: 0, 13, 5, 2 cases) ( χ2=20.17, P<0.05). Four cases of pulmonary artery dissection and one episode of hemoptysis occurred postoperatively, with no other complications reported. Conclusions:BPA can significantly improve exercise tolerance and hemodynamic parameters for residual PH after PEA. BPA is a relatively safe and effective treatment for residual PH after PEA.

Objective:To explore and analyze the clinical features of patients with immunoglobulin (Ig)G4-related hepatobiliary-pancreatic disease and the independent factors affecting the prognosis of IgG4-related sclerosing cholangitis (IgG4-SC).Methods:The clinical data of 179 adult cases diagnosed with IgG4-related hepato-pancreato-biliary disease in the Division of Gastroenterology and Hepatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine from January 2011 to December 2022 were retrospectively analyzed. Patients were divided into three groups: isolated IgG4-SC, IgG4-SC/type 1 autoimmune pancreatitis(type 1 AIP), and isolated AIP according to the clinical manifestations. Demographic characteristics, baseline biochemical immunological indexes, and imaging manifestations were analyzed. The treatment response rate and survival rate were compared. The COX proportional hazards model was used to analyze the independent factors related to prognosis.Results:The mean age of diagnosis of patients with IgG4-related hepatobiliary-pancreatic disease was 60.3±12.0 years. Males accounted for 74.9%, and the median follow-up time was 38 months. The 1-year clinical response rate of patients with isolated IgG4-SC was lower than that of IgG4-SC/AIP (67.9% vs. 91.7%, P=0.019), and the primary endpoint-free 5-year survival rate was significantly reduced (64.9% vs. 95.9%, P<0.001). COX regression analysis showed that having cirrhosis before treatment ( HR=6.708, P=0.004) and poor response after half a year of treatment ( HR=11.488, P=0.002) were independent risk factors associated with the occurrence of adverse events in hepatobiliary diseases among patients with IgG4-SC. Conclusions:The clinical response rate and survival rate of patients with isolated IgG4-SC are lower than those of patients with IgG4-SC/AIP. Patients with IgG4-SC who do not respond well at six months of treatment and who have progressed to cirrhosis before treatment are at significantly increased risk of adverse events.

Objective:To investigate the influences and mechanism of extracellular vesicles from dermal papilla cells (DPC-EVs) of mice on human hypertrophic scar fibroblasts (HSFs).Methods:The study was an experimental research. The primary dermal papilla cells (DPCs) of whiskers were extracted from 10 6-week-old male C57BL/6J mice and identified successfully. The DPC-EVs were extracted from the 3 rd to 5 th passage DPCs by ultracentrifugation, and the morphology was observed through transmission electron microscope and the particle diameter was detected by nanoparticle tracking analyzer ( n=3) at 24 h after culture. The 3 rd passage of HSFs were divided into DPC-EV group and phosphate buffer solution (PBS) group, which were cultured with DPC-EVs and PBS, respectively. The cell scratch test was performed and cell migration rate at 24 h after scratching was calculated ( n=5). The cell proliferation levels at 0 (after 12 h of starvation treatment and before adding DPC-EVs or PBS), 24, 48, 72, and 96 h after culture were detected by using cell counting kit 8 ( n=4). The protein expressions of α-smooth muscle actin (α-SMA) and collagen typeⅠ (ColⅠ) in cells at 24 h after culture were detected by immunofluorescence method and Western blotting, and the protein expression of Krüppel-like factor 4 (KLF4) in cells at 24 h after culture was detected by Western blotting. After the 3 rd passage of HSFs were cultured with DPC-EVs for 24 h, the cells were divided into blank control group, KLF4 knockdown group, and KLF4 overexpression group according to the random number table. The cells in blank control group were only routinely cultured for 48 h. The cells in KLF4 knockdown group and KLF4 overexpression group were incubated with KLF4 knockdown virus for 24 h, then the cells in KLF4 knockdown group were routinely cultured for 24 h while the cells in KLF4 overexpression group were incubated with KLF4 overexpression virus for 24 h. The protein expressions of KLF4, α-SMA, and ColⅠ in cells were detected by Western blotting at 48 h after culture. Results:At 24 h after culture, the extracted DPC-EVs showed vesicular structure with an average particle diameter of 108.8 nm. At 24 h after scratching, the migration rate of HSFs in PBS group was (54±10)%, which was significantly higher than (29±8)% in DPC-EV group ( t=4.37, P<0.05). At 48, 72, and 96 h after culture, the proliferation levels of HSFs in DPC-EV group were significantly lower than those in PBS group (with t values of 4.06, 5.76, and 6.41, respectively, P<0.05). At 24 h after culture, the protein expressions of α-SMA and ColⅠ of HSFs in DPC-EV group were significantly lower than those in PBS group, while the protein expression of KLF4 was significantly higher than that in PBS group. At 48 h after culture, compared with those in blank control group, the protein expression of KLF4 of HSFs in KLF4 knockdown group was down-regulated, while the protein expressions of α-SMA and ColⅠ were both up-regulated; compared with those in KLF4 knockdown group, the protein expression of KLF4 of HSFs in KLF4 overexpression group was up-regulated, while the protein expressions of ColⅠ and α-SMA were down-regulated. Conclusions:The DPC-EVs of mice can inhibit the proliferation and migration of human HSFs and significantly inhibit the expressions of fibrosis markers α-SMA and ColⅠ in human HSFs by activating KLF4.

Objective To investigate the role and potential mechanisms of tumor necrosis factor alpha-inducible protein 8-like molecule 1(TNFAIP8L1)in acute liver injury in mice.Methods The second generation of C57BL/6J male wild-type(WT)mice and the C57BL/6J female TNFAIP8L1+/-mice and WT mice were selected to further self-breed the third generation of male TNFAIP8L1-/-mice and the third generation of WT male mice.Five normal third-generation male WT mice and five normal third-generation male TNFAIP8L1-/-mice were selected.The serum alanine aminotransferase(ALT)levels of the two types of normal mice were measured and compared.The infiltration of inflammatory cells and cell necrosis in the liver tissues of the two types of normal mice were observed after hematoxylin & eosin(HE)staining.Flow cytometry was used to detect the percentages of neutrophils(Neu),eosinophils(EOS),dendritic cells(DC),bone marrow-derived macrophages(BMDMs),and bone marrow-derived mononuclear cell(BMNCs)in the liver myeloid cell subsets of the two types of normal mice.Another 5 third-generation male WT mice and 4 third-generation male TNFAIP8L1-/-mice were selected to induce acute liver injury mouse models using lipopolysaccharide(LPS)/D-galactosamine(D-Gal).After 24 hours,the serum ALT levels of the two types of acute liver injury mice were detected and compared,the infiltration of inflammatory cells and cell necrosis in the liver tissues of the two types of acute liver injury mice were observed,and the percentages of Neu,EOS,DC,BMDMs and BMNCs in the liver myeloid cell subsets of the two types of acute liver injury mice were measured by using the above methods.Results There was no significant difference in the percentages of Neu,EOS,DC,BMDMs and BMNCs,and serum ALT levels in the livermyeloid cell subsets of normal WT mice and TNFAIP8L1-/-mice(P＞0.05).HE staining results of liver tissues in normal WT mice and TNFAIP8L1/mice showed that hepatic lobules were structurally complete and clear,hepatocytes were morphologically normal and arranged neatly,and there was no obvious inflammatory cell infiltration or cell necrosis.Twenty-four hours after acute liver injury,the percentages of Neu and BMNCs in the liver myeloid cell subsets and the serum ALT levels in the liver tissues of TNFAIP8L1-/-mice were significantly higher than those of WT mice(P＜0.05);there was no significant difference in the percentages of EOS,DC and BMDMs in the liver myeloid cell subsets of mice between the two groups(P＞0.05).In the liver tissues of WT mice with acute liver injury,hepatic lobules were structurally blurred,hepatocytes were swollen with scattered vacuolated steatosis,and a small amount of inflammatory cells were infiltrated.In the liver tissues of TNFAIP8L1/mice with acute liver injury,hepatic lobules were structurally non-existent,and hepatocytes were severely damaged and extensively necrotic,with a large amount of inflammatory cell infiltration.Conclusion The deficiency of the TNFAIP8L1 gene in mice does not affect the development of liver myeloid cells and the homeostasis of the liver.TNFAIP8L1 plays an inhibitory role in the occurrence and development of acute liver injury.TNFAIP8L1 gene deficiency aggravates LPS/D-Gal-induced acute liver injury,possibly by increasing Neu and BMNCs infiltration and recruiting other types of immune cells to infiltrate liver tissues,thereby exacerbating liver cell necrosis.

Objective To investigate the role of proanthocyanidins (PC) in lipopolysaccharide (LPS)-induced inflammatory response and its possible mechanism in RAW264.7 macrophages. Methods RAW264.7 macrophages were cultured and treated with PBS and different concentrations of PC for 24 hours, followed by 1 μg/mL LPS for 6 hours. Real-time PCR was used to detect the mRNA expression of interleukin1β (IL-1β), IL-6, monocyte chemoattractant protein 1 (MCP-1), tumor necrotic factor α (TNF-α), IL-4 and arginase 1 (Arg1) in RAW264.7 macrophages. Flow cytometry was used to detect the effects of PBS group, LPS group and PC combined with LPS group on M1 and M2 polarization of macrophages. The protein expressions of silenced information regulator 1 (SIRT1), nuclear factor kappa B p65(NF-κB p65) and acetylated NF-κB p65 (Ace-p65) were detected by Western blot analysis after different concentrations of PC treatment. Co-immunoprecipitation assay was used to detect the binding effect of SIRT1 to NF-κB p65 in macrophages treated with PC. Results Compared with PBS group, the mRNA expression of macrophage pro-inflammatory cytokines IL-1β, IL-6, MCP-1 and TNF-α decreased and the mRNA expression of anti-inflammatory factors IL-4 and Arg1 increased in PC group. Compared with LPS group, PC combined with LPS group could significantly inhibit M1 polarization and promote M2 polarization of macrophages. With the increase of PC concentration, the expression of SIRT1 was up-regulated, and NF-κB p65 protein did not change significantly. The expression of Ace-p65 protein decreased significantly when treated with high concentration of PC. Conclusion PC can significantly alleviate the LPS-induced inflammatory response by up-regulating the expression of SIRT1 and inhibiting NF-κB pathway in RAW264.7 macrophages.
Animals ; Mice ; Interleukin-4 ; Interleukin-6 ; Lipopolysaccharides ; Macrophages ; NF-kappa B ; Proanthocyanidins ; RNA, Messenger ; Sirtuin 1/genetics* ; Tumor Necrosis Factor-alpha ; RAW 264.7 Cells

Colorectal cancer is a disease with high morbidity and mortality. Colorectal cancer has a poor prognosis, duing to the current limited treatment methods and can not achieve satisfactory treatment results. Therefore, how to diagnose colorectal cancer patients early and improve the prognosis has always been one of the problems in the medical and scientific research circles. As researchers gradually learn more about the intestinal flora including Fusobacterium nucleatum, the targeted treatment has been applied to the experimental research and clinical treatment of colorectal cancer. This paper reviews the research progress of Fusobacterium nucleatum on the pathogenesis, early diagnosis, prognosis and treatment of colorectal cancer in recent years.

Objective:To observe the effect of pressure therapy on the formation of hypertrophic scars(HTS) and transforming growth factor beta 1 (TGF-β1) / Sma and Mad homolog proteins (Smad) signaling pathway.Methods:Twelve adult healthy New Zealand white rabbits(provided by the Animal Experiment Center of the Air Force Military Medical University) were wounded with 1 cm round punch on 4 sites of the ventral side of each ear. Round scalpels were used to make incisions along the marked lines, dissect the skin and perichondrium. The remaining tissue was scraped off to expose the wound surface. Scar formation was observed on the 28th day after surgery. After the establishment of rabbit ear HTS models, the right ears were used as self-controls, while the left ears were set as the experimental group. Two hypertrophic scars were randomly selected from each rabbit ear, 24 per group. Experimental group: 4-0 nylon silk thread was used to sew the pressure pad on the circular NdFeB magnets pad with a diameter of 1.5 cm to the rabbit ear cartilage. Flexiforce pressure sensor was used to measure the pressure, and the pads were adjusted to maintain a pressure of 20-25 mmHg (1 mmHg=0.133 kPa) for more than 23 h per day. Control group: no treatment. On the 40th day of pressure therapy, the general morphology of rabbit ear scars were observed, and the tissues were harvested for hematoxylin and eosin (HE) staining and Masson’s Trichrome staining for histological study. The scar elevation index (SEI), the number of fibroblasts, and the thickness of the stratum corneum were calculated. The relative mRNA expression levels of TGF-β1, Smad3, collagen type (Collagen )Ⅰ, Collagen Ⅲ, α-smooth muscle actin (α-SMA) were measured with qPCR; Western blotting was used to detect the relative protein expression levels of TGF-β1, Collagen Ⅰ, Collagen Ⅲ, α-SMA and the phosphorylation level of Smad3 (the ratio of p-Smad3 and Smad3 proteins). Statistical analysis was performed with Excel 2019 and GraphPad Prism 8.0. The measurement data conformed to normal distribution and was expressed as Mean±SD. Student’s t-test was used for the comparison between two groups. P<0.05 was considered statistically significant. Results:A total of 96 wounds were formed in 12 rabbits, 27 wounds had no obvious hyperplasia, and the remaining 69 wounds formed hypertrophic scar tissue blocks with a prominent skin surface, firm texture, and dark red appearance. The scars formation rate was 71.9% (69/96). On the 40th day after the application of pressure, the scars in the experimental group were significantly reduced, softer, and the color was slightly lighter compared with the control group. The results of HE staining and Masson’s Trichrome staining showed that the thickness of the stratum corneum, SEI, and the number of fibroblasts were (69.33±6.03) μm, 1.30±0.08, and (236.30±14.64) cells/field, respectively, which were significantly lower than those in the control group [(114.00±10.15) μm, 1.72±0.05, (320.30±14.57) cells/field] (all P<0.01). Abundance in capillaries, inflammatory cells, and fibroblasts were not observed in the dermal layer. The collagen fibers were orderly arranged and sparse. The results of fluorescence quantitative PCR showed that the relative expression levels of TGF-β1, Smad3, Collagen Ⅰ, Collagen Ⅲ, and α-SMA mRNA in the experimental group were 0.48±0.08, 0.58±0.05, 0.04±0.01, 0.15±0.02, 0.31±0.03, respectively, lower than those of the control group(1.00±0.07, 1.00±0.05, 1.00±0.08, 1.00±0.10, 1.00±0.06) (all P<0.01). The results of Western blotting showed that the relative protein expression of TGF-β1, Collagen Ⅰ, Collagen Ⅲ, α-SMA and the phosphorylation level of Smad3 in the experimental group were 0.65±0.03, 0.07±0.01, 0.43±0.03, 0.53±0.03, 0.54±0.03, all lower than the control group’s 1.02±0.06, 0.93±0.05, 0.92±0.03, 0.82±0.03, 0.92±0.03 (all P<0.01). Conclusions:Pressure therapy can significantly inhibit the hyperplasia of scars, improve the structure of HTS tissue, facilitate the normal arrangement of collagen fiber, and reduce the excessive deposition of collagen. Pressure therapy may inhibit scar proliferation by regulating the TGF-β1/Smad signaling pathway.

Objective:To observe the effect of pressure therapy on the formation of hypertrophic scars(HTS) and transforming growth factor beta 1 (TGF-β1) / Sma and Mad homolog proteins (Smad) signaling pathway.Methods:Twelve adult healthy New Zealand white rabbits(provided by the Animal Experiment Center of the Air Force Military Medical University) were wounded with 1 cm round punch on 4 sites of the ventral side of each ear. Round scalpels were used to make incisions along the marked lines, dissect the skin and perichondrium. The remaining tissue was scraped off to expose the wound surface. Scar formation was observed on the 28th day after surgery. After the establishment of rabbit ear HTS models, the right ears were used as self-controls, while the left ears were set as the experimental group. Two hypertrophic scars were randomly selected from each rabbit ear, 24 per group. Experimental group: 4-0 nylon silk thread was used to sew the pressure pad on the circular NdFeB magnets pad with a diameter of 1.5 cm to the rabbit ear cartilage. Flexiforce pressure sensor was used to measure the pressure, and the pads were adjusted to maintain a pressure of 20-25 mmHg (1 mmHg=0.133 kPa) for more than 23 h per day. Control group: no treatment. On the 40th day of pressure therapy, the general morphology of rabbit ear scars were observed, and the tissues were harvested for hematoxylin and eosin (HE) staining and Masson’s Trichrome staining for histological study. The scar elevation index (SEI), the number of fibroblasts, and the thickness of the stratum corneum were calculated. The relative mRNA expression levels of TGF-β1, Smad3, collagen type (Collagen )Ⅰ, Collagen Ⅲ, α-smooth muscle actin (α-SMA) were measured with qPCR; Western blotting was used to detect the relative protein expression levels of TGF-β1, Collagen Ⅰ, Collagen Ⅲ, α-SMA and the phosphorylation level of Smad3 (the ratio of p-Smad3 and Smad3 proteins). Statistical analysis was performed with Excel 2019 and GraphPad Prism 8.0. The measurement data conformed to normal distribution and was expressed as Mean±SD. Student’s t-test was used for the comparison between two groups. P<0.05 was considered statistically significant. Results:A total of 96 wounds were formed in 12 rabbits, 27 wounds had no obvious hyperplasia, and the remaining 69 wounds formed hypertrophic scar tissue blocks with a prominent skin surface, firm texture, and dark red appearance. The scars formation rate was 71.9% (69/96). On the 40th day after the application of pressure, the scars in the experimental group were significantly reduced, softer, and the color was slightly lighter compared with the control group. The results of HE staining and Masson’s Trichrome staining showed that the thickness of the stratum corneum, SEI, and the number of fibroblasts were (69.33±6.03) μm, 1.30±0.08, and (236.30±14.64) cells/field, respectively, which were significantly lower than those in the control group [(114.00±10.15) μm, 1.72±0.05, (320.30±14.57) cells/field] (all P<0.01). Abundance in capillaries, inflammatory cells, and fibroblasts were not observed in the dermal layer. The collagen fibers were orderly arranged and sparse. The results of fluorescence quantitative PCR showed that the relative expression levels of TGF-β1, Smad3, Collagen Ⅰ, Collagen Ⅲ, and α-SMA mRNA in the experimental group were 0.48±0.08, 0.58±0.05, 0.04±0.01, 0.15±0.02, 0.31±0.03, respectively, lower than those of the control group(1.00±0.07, 1.00±0.05, 1.00±0.08, 1.00±0.10, 1.00±0.06) (all P<0.01). The results of Western blotting showed that the relative protein expression of TGF-β1, Collagen Ⅰ, Collagen Ⅲ, α-SMA and the phosphorylation level of Smad3 in the experimental group were 0.65±0.03, 0.07±0.01, 0.43±0.03, 0.53±0.03, 0.54±0.03, all lower than the control group’s 1.02±0.06, 0.93±0.05, 0.92±0.03, 0.82±0.03, 0.92±0.03 (all P<0.01). Conclusions:Pressure therapy can significantly inhibit the hyperplasia of scars, improve the structure of HTS tissue, facilitate the normal arrangement of collagen fiber, and reduce the excessive deposition of collagen. Pressure therapy may inhibit scar proliferation by regulating the TGF-β1/Smad signaling pathway.

Objective:To explore the effects of mechanical tension on the formation of hypertrophic scars in rabbit ears and transforming growth factor-β 1 (TGF-β 1)/Smad signaling pathway. Methods:The experimental research method was adopted. Six New Zealand white rabbits, male or female, aged 3-5 months were used and 5 full-thickness skin defect wounds were made on the ventral surface of each rabbit ear. The appearance of all rabbit ear wounds was observed on post surgery day (PSD) 0 (immediately), 7, 14, 21, and 28. On PSD 28, the scar formation rate was calculated. Three mature scars in the left ear of each rabbit were included in tension group and the arch was continuously expanded with a spiral expander. Three mature scars in the right ear of each rabbit were included in sham tension group and only the spiral expander was sutured without expansion. There were 18 scars in each group. After mechanical tension treatment (hereinafter referred to as treatment) for 40 days, the color and texture of scar tissue in the two groups were observed. On treatment day 40, the scar elevation index (SEI) was observed and calculated; the histology was observed after hematoxylin eosin staining, and the collagen morphology was observed after Masson staining; mRNA expressions of TGF-β 1, Smad3, collagen Ⅰ, collagen Ⅲ, and α-smooth muscle actin (α-SMA) in scar tissue were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction; and the protein expressions of TGF-β 1, collagen Ⅰ, collagen Ⅲ, and α-SMA, and phosphorylation level of Smad3 in scar tissue were detected by Western blotting. The number of samples of each group in the experiments was 3. Data were statistically analyzed with independent sample t test. Results:On PSD 0, 5 fresh wounds were formed on all the rabbit ears; on PSD 7, the wounds were scabbed; on PSD 14, most of the wounds were epithelialized; on PSD 21, all the wounds were epithelialized; on PSD 28, obvious hypertrophic scars were formed. The scar formation rate was 75% (45/60) on PSD 28. On treatment day 40, the scar tissue of rabbit ears in tension group was more prominent than that in sham tension group, the scar tissue was harder and the color was more ruddy; the SEI of the scar tissue of rabbit ears in tension group (2.02±0.08) was significantly higher than 1.70±0.08 in sham tension group ( t=5.07, P<0.01). On treatment day 40, compared with those in sham tension group, the stratum corneum of scar tissue became thicker, and a large number of new capillaries, inflammatory cells, and fibroblasts were observed in the dermis, and collagen was more disordered, with nodular or swirling distribution in the scar tissue of rabbit ears in tension group. On treatment day 40, the mRNA expressions of TGF-β 1, Smad3, collagen Ⅰ, collagen Ⅲ, and α-SMA in the scar tissue of rabbit ears in tension group were respectively 1.81±0.25, 5.71±0.82, 7.86±0.56, 4.35±0.28, and 5.89±0.47, which were significantly higher than 1.00±0.08, 1.00±0.12, 1.00±0.13, 1.00±0.14, and 1.00±0.14 in sham tension group (with t values of 5.36, 9.82, 20.60, 18.26, and 17.13, respectively, all P<0.01); the protein expressions of TGF-β 1, collagen Ⅰ, collagen Ⅲ, and α-SMA, and phosphorylation level of Smad3 in the scar tissue of rabbit ears in tension group were respectively 0.865±0.050, 0.895±0.042, 0.972±0.027, 1.012±0.057, and 0.968±0.087, which were significantly higher than 0.657±0.050, 0.271±0.029, 0.631±0.027, 0.418±0.023, and 0.511±0.035 in sham tension group (with t values of 5.08, 21.27, 15.55, 16.70, and 8.40, respectively, all P<0.01). Conclusions:Mechanical tension can inhibit the regression of hypertrophic scars in rabbit ears through stimulating the hyperplasia of scars, inhibiting the normal arrangement of dermal collagen fibers, and intensifying the deposition of collagen fibers, and the mechanism may be related to the activation of TGF-β 1/Smad signaling pathway by mechanical tension.