Effect and mechanism of hyperbaric oxygen on chronic wounds of full-thickness skin defects in rats
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摘要:
目的 探讨高压氧对大鼠全层皮肤缺损慢性创面的作用及其机制。 方法 该研究为成组设计实验研究。取40只3个月龄雄性SD大鼠,按照随机数字表法分为对照组、模型组、高压氧组、铁抑素-1组,每组10只。对照组大鼠背部仅接受全层皮肤切除；模型组大鼠在背部全层皮肤切除后肌内注射醋酸氢化可的松建立慢性创面；高压氧组与铁抑素-1组大鼠在背部全层皮肤切除及肌内注射醋酸氢化可的松的基础上,分别接受高压氧治疗和铁抑素-1干预。治疗7 d后,观察大鼠创面情况并计算其愈合率,采用苏木精-伊红染色检测创面组织的病理情况并进行评分,通过透射电子显微镜观察创面组织中成纤维细胞（Fb）的超微结构,采用酶联免疫吸附测定法检测创面组织中白细胞介素-1β（IL-1β）、IL-6、基质金属蛋白酶-9、基质金属蛋白酶组织抑制因子-1的表达水平,采用相关试剂盒检测创面组织中丙二醛、谷胱甘肽、超氧化物歧化酶的含量,采用免疫荧光法和蛋白质印迹法检测创面组织中核转录因子红系2相关因子2（Nrf2）、溶质载体家族7成员11（SLC7A11）、谷胱甘肽过氧化物酶4（GPX4）的表达情况。 结果 治疗7 d后,各组大鼠创面均出现红肿、渗出,以模型组溃烂最为明显；模型组大鼠创面上皮化进程亦明显滞后于高压氧组、铁抑素-1组和对照组。治疗7 d后,高压氧组、铁抑素-1组和对照组大鼠创面愈合率均明显高于模型组（P<0.05）。治疗7 d后,各组大鼠创面组织均存在不同程度的水肿和炎性浸润,以模型组最为明显；高压氧组、铁抑素-1组和对照组大鼠创面组织病理评分均明显高于模型组（P<0.05）。治疗7 d后,对照组大鼠创面组织中Fb的线粒体结构完整；模型组大鼠创面组织中Fb的线粒体缩小,线粒体嵴消失,外膜破裂；高压氧组和铁抑素-1组大鼠创面组织中Fb的线粒体损伤较轻。治疗7 d后,与模型组相比,高压氧组、铁抑素-1组和对照组大鼠创面组织中IL-1β、IL-6、基质金属蛋白酶-9的表达水平均明显降低（P<0.05）,而基质金属蛋白酶组织抑制因子-1的表达水平均明显升高（P<0.05）。治疗7 d后,与模型组相比,高压氧组、铁抑素-1组和对照组大鼠创面组织中丙二醛含量均明显降低（P<0.05）,而谷胱甘肽、超氧化物歧化酶含量均明显升高（P<0.05）。治疗7 d后,免疫荧光法检测显示,模型组大鼠创面组织中Nrf2、SLC7A11、GPX4的表达水平分别为10.1±1.4、23.2±1.9、19.7±1.3,均明显低于高压氧组的20.6±1.8、32.9±1.7、31.6±3.0,铁抑素-1组的21.2±2.4、31.1±2.7、32.2±1.2和对照组的27.8±1.6、39.4±2.1、39.4±2.0,P<0.05；蛋白质印迹法检测显示,模型组大鼠创面组织中Nrf2、SLC7A11、GPX4的表达水平分别为0.72±0.06、0.56±0.05、0.69±0.03,均明显低于高压氧组的0.88±0.03、0.90±0.07、0.85±0.06,铁抑素-1组的0.86±0.06、0.77±0.09、0.87±0.03和对照组的0.90±0.04、0.82±0.04、0.87±0.04,P<0.05。 结论 高压氧能有效促进大鼠全层皮肤缺损慢性创面愈合,其作用机制可能与激活铁死亡抑制分子Nrf2、SLC7A11、GPX4的表达,从而减轻炎症反应和氧化应激有关。 Abstract:Objective To investigate the effect and mechanism of hyperbaric oxygen on chronic wounds of full-thickness skin defects in rats. Methods This study was designed as grouped experimental study. Forty 3-month-old male Sprague-Dawley rats were divided into control group, model group, hyperbaric oxygen group, and ferrostatin-1 group using a random number table method, with 10 rats in each group. Rats in control group only received full-thickness skin excision on the back. Rats in model group received an intramuscular injection of hydrocortisone acetate after full-thickness skin excision on the back to establish chronic wounds. In addition to full-thickness skin excision on the back and intramuscular injection of hydrocortisone acetate, rats in hyperbaric oxygen group and in ferrostatin-1 group received hyperbaric oxygen therapy and ferrostatin-1 intervention, respectively. After 7 days of treatment, the wound condition was observed and the wound healing rate was calculated. Hematoxylin-eosin staining was used to detect the pathological changes of wound tissue and scored. Transmission electron microscopy was used to observe the ultrastructure of fibroblasts (Fbs) in the wound tissue. Enzyme-linked immunosorbent assay was used to detect the expression levels of interleukin-1β (IL-1β), IL-6, matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of MMP-1 (TIMP-1) in the wound tissue. Relevant kits were used to determine the content of malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) in the wound tissue. Immunofluorescence and Western blotting were used to detect the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), solute carrier family 7 member 11 (SLC7A11), and glutathione peroxidase 4 (GPX4) in the wound tissue. Results After 7 days of treatment, the wounds in all groups of rats exhibited redness, swelling, and exudation, with the most pronounced ulceration observed in model group; the process of wound epithelialization of rats in model group was also significantly delayed compared with that in hyperbaric oxygen group, ferrostatin-1 group, and control group. After 7 days of treatment, the wound healing rates of rats in hyperbaric oxygen group, ferrostatin-1 group, and control group were significantly higher than that in model group (P<0.05). After 7 days of treatment, varying degrees of edema and inflammatory infiltration were observed in the wound tissue of rats in all groups, with the most severe changes being observed in model group. The histopathological scores of wound tissue of rats in hyperbaric oxygen group, ferrostatin-1 group, and control group were significantly higher than that in model group (P<0.05). After 7 days of treatment, the mitochondrial structure of Fbs in the wound tissue of rats in control group was intact. In model group, the Fbs mitochondria in the wound tissue of rats were shrunken, the mitochondrial cristae disappeared and the outer membrane of mitochondria ruptured. In hyperbaric oxygen group and ferrostatin-1 group, the Fbs mitochondrial damage in the wound tissue of rats was mild. After 7 days of treatment, compared with those in model group, the expression levels of IL-1β, IL-6, and MMP-9 in the wound tissue of rats in hyperbaric oxygen group, ferrostatin-1 group, and control group were significantly decreased (P<0.05), while the expression levels of TIMP-1 were significantly increased (P<0.05). After 7 days of treatment, compared with that in model group, the MDA content in the wound tissue of rats in hyperbaric oxygen group, ferrostatin-1 group, and control group was significantly decreased (P<0.05), while the content of GSH and SOD was significantly increased (P<0.05). After 7 days of treatment, immunofluorescence detection showed that the expression levels of Nrf2, SLC7A11, and GPX4 in the wound tissue of rats in model group were 10.1±1.4, 23.2±1.9, and 19.7±1.3, respectively, which were significantly lower than those in hyperbaric oxygen group (20.6±1.8, 32.9±1.7, and 31.6±3.0, respectively), ferrostatin-1 group (21.2±2.4, 31.1±2.7, and 32.2±1.2, respectively), and control group (27.8±1.6, 39.4±2.1, and 39.4±2.0, respectively), P<0.05; Western blotting detection revealed that the expression levels of Nrf2, SLC7A11, and GPX4 in the wound tissue of rats in model group were 0.72±0.06, 0.56±0.05, and 0.69±0.03, respectively, which were significantly lower than those in hyperbaric oxygen group (0.88±0.03, 0.90±0.07, and 0.85±0.06, respectively), ferrostatin-1 group (0.86±0.06, 0.77±0.09, and 0.87±0.03, respectively), and control group (0.90±0.04, 0.82±0.04, and 0.87±0.04, respectively), P<0.05. Conclusions Hyperbaric oxygen can effectively promote the healing of chronic wounds of full-thickness skin defects in rats, and its mechanism may be related to activating the expression of ferroptosis inhibitory molecules Nrf2, SLC7A11, and GPX4, thereby reducing inflammatory response and oxidative stress. -
Key words:
- Hyperbaric oxygenation /
- Oxidative stress /
- Inflammation /
- Ferroptosis /
- Chronic wounds /
- Lipid peroxidation /
- Wound repair
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参考文献
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图 1 4组大鼠全层皮肤缺损创面治疗前及治疗7 d后的愈合情况。1A、1B、1C、1D.分别为对照组、模型组、高压氧组、铁抑素-1组大鼠皮肤切除即刻的新鲜创面；1E、1F、1G、1H.分别为对照组、模型组、高压氧组、铁抑素-1组大鼠创面治疗7 d后的愈合情况,各组大鼠创面均红肿,渗出,表面有坏死组织覆盖,少许肉芽组织形成,其中以图1F创面溃烂最为明显
注：对照组大鼠仅接受全层皮肤切除；模型组大鼠在全层皮肤切除后肌内注射醋酸氢化可的松建立慢性创面；高压氧组与铁抑素-1组大鼠在全层皮肤切除及肌内注射醋酸氢化可的松的基础上,分别接受高压氧治疗和铁抑素-1干预
图 2 4组大鼠全层皮肤缺损创面治疗7 d后的组织病理情况及成纤维细胞的超微结构。2A、2B、2C、2D.分别为对照组、模型组、高压氧组、铁抑素-1组大鼠创面治疗7 d后的组织病理情况,红色箭头所指为新生血管,蓝色箭头所指为炎症部位,黑色箭头所指为水肿部位,图2B中水肿和炎性浸润最为明显 苏木精-伊红 ×100；2E、2F、2G、2H.分别为对照组、模型组、高压氧组、铁抑素-1组大鼠创面治疗7 d后组织中细胞的超微结构,绿色箭头所指为线粒体,图2E中成纤维细胞的线粒体结构正常,图2F中成纤维细胞的线粒体缩小且线粒体嵴消失,图2G和图2H中成纤维细胞的线粒体损伤较轻 透射电子显微镜 ×20 000
注：对照组大鼠仅接受全层皮肤切除；模型组大鼠在全层皮肤切除后肌内注射醋酸氢化可的松建立慢性创面；高压氧组与铁抑素‑1组大鼠在全层皮肤切除及肌内注射醋酸氢化可的松的基础上,分别接受高压氧治疗和铁抑素‑1干预
图 3 4组大鼠全层皮肤缺损创面治疗7 d后铁死亡抑制分子的表达情况 花青素3-4',6-二脒基-2-苯基吲哚 ×400。3A、3B、3C、3D.分别为对照组、模型组、高压氧组、铁抑素-1组大鼠创面中核转录因子红系2相关因子2表达情况,图3B的表达最低；3E、3F、3G、3H.分别为对照组、模型组、高压氧组、铁抑素-1组大鼠创面中溶质载体家族7成员11表达情况,图3F的表达最低；3I、3J、3K、3L.分别为对照组、模型组、高压氧组、铁抑素-1组大鼠创面中谷胱甘肽过氧化物酶4表达情况,图3J的表达最低
注：对照组大鼠仅接受全层皮肤切除；模型组大鼠在全层皮肤切除后肌内注射醋酸氢化可的松；高压氧组与铁抑素‑1组大鼠在全层皮肤切除及肌内注射醋酸氢化可的松的基础上,分别接受高压氧治疗和铁抑素‑1干预；细胞核染色为蓝色,各分子阳性染色为红色
图 4 蛋白质印迹法检测的4组大鼠全层皮肤缺损创面治疗7 d后铁死亡抑制分子的表达情况。4A、4B、4C.分别为Nrf2、SLC7A11、GPX4的条带图；4D.条图
注：图4A、4B、4C条带图上方的1、2、3、4均分别指对照组、模型组、高压氧组、铁抑素‑1组；对照组大鼠仅接受全层皮肤切除；模型组大鼠在全层皮肤切除后肌内注射醋酸氢化可的松建立慢性创面；高压氧组与铁抑素‑1组大鼠在全层皮肤切除及肌内注射醋酸氢化可的松的基础上,分别接受高压氧治疗和铁抑素‑1干预；Nrf2为核转录因子红系2相关因子2,GAPDH为3‑磷酸甘油醛脱氢酶,SLC7A11为溶质载体家族7成员11,GPX4为谷胱甘肽过氧化物酶4；与模型组相比,aP<0.05
Table 1. 4组大鼠全层皮肤缺损创面治疗7 d后创面修复相关分子表达水平比较（
组别 样本数 IL-1β（pg/mg） IL-6（pg/mg） MMP-9（pg/mg） TIMP-1（pg/µg） 对照组 3 13.7±0.8 17.2±0.8 283±42 1.88±0.11 模型组 3 19.7±0.9 35.9±4.1 447±20 1.53±0.06 高压氧组 3 15.6±0.8 24.9±4.2 375±17 1.91±0.11 铁抑素-1组 3 15.1±1.6 23.2±2.2 299±14 1.90±0.08 F值 17.36 18.61 25.89 11.78 P值 0.001 0.001 <0.001 0.003 P1值 <0.001 <0.001 <0.001 0.005 P2值 0.004 0.007 0.022 0.003 P3值 0.002 0.003 <0.001 0.003 注：IL为白细胞介素,MMP-9为基质金属蛋白酶-9,TIMP-1为MMP组织抑制因子-1；对照组大鼠仅接受全层皮肤切除；模型组大鼠在全层皮肤切除后肌内注射醋酸氢化可的松建立慢性创面；高压氧组与铁抑素-1组大鼠在全层皮肤切除及肌内注射醋酸氢化可的松的基础上,分别接受高压氧治疗和铁抑素-1干预；F值、P值为4组间各指标总体比较所得；P1值、P2值、P3值分别为对照组、高压氧组、铁抑素-1组各指标与模型组比较所得 
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Table 2. 4组大鼠全层皮肤缺损创面治疗7 d后脂质过氧化相关分子表达水平比较（
组别 样本数 丙二醛（µmol/g） 谷胱甘肽（µmol/g） SOD（U/mg） 对照组 3 4.4±1.2 16.0±2.2 111±5 模型组 3 12.0±1.7 7.9±0.4 66±11 高压氧组 3 8.1±1.1 12.4±1.1 88±7 铁抑素-1组 3 7.8±1.7 11.7±0.5 88±7 F值 13.92 19.99 16.76 P值 0.002 <0.001 0.001 P1值 0.001 <0.001 <0.001 P2值 0.028 0.006 0.023 P3值 0.018 0.017 0.024 注：SOD为超氧化物歧化酶；对照组大鼠仅接受全层皮肤切除；模型组大鼠在全层皮肤切除后肌内注射醋酸氢化可的松建立慢性创面；高压氧组与铁抑素-1组大鼠在全层皮肤切除及肌内注射醋酸氢化可的松的基础上,分别接受高压氧治疗和铁抑素-1干预；F值、P值为4组间各指标总体比较所得；P1值、P2值、P3值分别为对照组、高压氧组、铁抑素-1组各指标与模型组比较所得
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Table 3. 4组大鼠全层皮肤缺损创面治疗7 d后铁死亡抑制分子的表达比较（
组别 样本数 Nrf2 SLC7A11 GPX4 对照组 3 27.8±1.6 39.4±2.1 39.4±2.0 模型组 3 10.1±1.4 23.2±1.9 19.7±1.3 高压氧组 3 20.6±1.8 32.9±1.7 31.6±3.0 铁抑素-1组 3 21.2±2.4 31.1±2.7 32.2±1.2 F值 46.28 29.82 50.40 P值 <0.001 <0.001 <0.001 P1值 <0.001 <0.001 <0.001 P2值 <0.001 0.001 <0.001 P3值 <0.001 0.005 <0.001 注：Nrf2为核转录因子红系2相关因子2,SLC7A11为溶质载体家族7成员11,GPX4为谷胱甘肽过氧化物酶4；对照组大鼠仅接受全层皮肤切除；模型组大鼠在全层皮肤切除后肌内注射醋酸氢化可的松建立慢性创面；高压氧组与铁抑素-1组大鼠在全层皮肤切除及肌内注射醋酸氢化可的松的基础上,分别接受高压氧治疗和铁抑素-1干预；F值、P值为4组间各指标总体比较所得；P1值、P2值、P3值分别为对照组、高压氧组、铁抑素-1组各指标与模型组比较所得
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