Nuclear factor E2-related factor 2 (Nrf2) is a major regulator of redox homeostasis in cells, and Nrf2 signaling pathway has anti-inflammatory, anti-oxidative stress, and anti-fibrosis effects while plays an important role in wound healing and pathological scar formation and progression. This article reviewed the related research regarding the effect of oxidative stress and Nrf2 signaling pathway on pathological scars, furthermore, it investigated the relationship between Nrf2 signaling pathway, oxidative stress and pathological scars, providing a new perspective for the study of mechanism and clinical prevention and treatments of pathological scars.

The sympathetic nervous system(SNS)plays a pivotal role in maintaining organ homeosta-sis and the pathogenesis of various ailments.Studies have unveiled a profound interconnection between sympathet-ic nerves and the development of liver cirrhosis,cirrhotic cardiomyopathy,and hepatorenal syndrome.Therefore,researchers have proposed SNS as a candidate therapeutic target for liver-related disorders.This article reviewed the research progress of sympathetic nerves in liver cirrhosis,cirrhotic cardiomyopathy,and hepatorenal syn-drome,aiming to enrich the knowledge about the roles of sympathetic nerves in cirrhosis and its complications and provide new ideas for the treatment of liver cirrhosis and its complications.

Nuclear factor E2-related factor 2 (Nrf2) is a major regulator of redox homeostasis in cells, and Nrf2 signaling pathway has anti-inflammatory, anti-oxidative stress, and anti-fibrosis effects while plays an important role in wound healing and pathological scar formation and progression. This article reviewed the related research regarding the effect of oxidative stress and Nrf2 signaling pathway on pathological scars, furthermore, it investigated the relationship between Nrf2 signaling pathway, oxidative stress and pathological scars, providing a new perspective for the study of mechanism and clinical prevention and treatments of pathological scars.

Objective:To investigate the related factors of perioperative venous thromboembolism (VTE) in inpatients of plastic surgery and to take individualized preventive measures to reduce the incidence of perioperative VTE in clinical practice.Methods:From January 2021 to June 2021, 127 patients without VTE were hospitalized in the Department of Plastic Surgery of the First Affiliated Hospital of Xinjiang Medical University, including 72 males and 55 females, aged 18-88 (62.2±14.0) years. The patients were divided into 23 cases in the VTE group and 104 cases in the non-VTE group according to whether VTE occurred in the perioperative period. The general data, etiology, underlying diseases, treatment modalities and blood indexes of the two groups were analyzed to summarize the independent influencing factors of VTE occurring in the perioperative period in plastic surgery.Results:Age, hypertension, diabetes, chronic skin ulcers, and length of surgery were risk factors associated with the development of perioperative VTE, (&chi; 2/ t=17.77, 8.24, 5.22, 25.55, 2.82, P<0.05). BMI ≥ 24 kg/m 2, general anaesthesia and short braking days were independent factors influencing the development of VTE in the perioperative period in plastic surgery inpatients, OR values were 8.908, 13.197, 0.042; P<0.05, respectively. Conclusions:BMI ≥ 24 kg/m 2 and general anaesthesia are the independent risk factors of plastic surgery in perioperative period developing VTE, short braking days is a protective factor against VTE in the perioperative period of plastic surgery. Clinicians should adequately assess the occurrence of perioperative VTE in plastic surgery inpatients and give early and individualized preventive measures.

Objective:To understand the iron content and transferrin receptor 1 (TfR1) expression levels in keloid and normal skin tissues, an in vitro model of keloid fibroblasts (KFB) ferroptosis induced by Erastin was constructed, and the effects of Erastin and Ferrostatin-1(Fer-1) on cell viability, ferrous ion (Fe 2+) content and lipid peroxidation, ferroptosis and fibrosis-related regulatory factors were examined. Methods:Six keloid tissues and six normal skin tissues were collected from the First Affiliated Hospital of Xinjiang Medical University from March to June 2022, and the tissue iron content kit was used to determine the iron content in the dermis of the two tissues, and TfR1 protein expression was detected in the two tissues by Western blot. Primary KFB and normal skin fibroblasts (NFB) were obtained by tissue block culture method, and the effect of different concentrations of Erastin and Fer-1 on cell activity was detected by using Erastin-induced KFB ferroptosis model and CCK-8 method to screen the appropriate drug concentration. The follow-up experiments were divided into five groups: NFB group, control group, Erastin (0.6 μmol/L) group, Fer-1 (1 μmol/L) group, and Erastin (0.6 μmol/L) +Fer-1 (1 μmol/L) group, while KFB was used as the experimental object in the last 4 groups. Cell migration ability was detected by scratch assay, and malondialdehyde (MDA), reactive oxygen species (ROS) and Fe 2+ content in each group of cells were detected by fluorescent probe method and kits; the protein expression of TfR1, glutathione peroxidase 4 (GPx4), solute carrier family 7 member 11 (SLC7A11), α-smooth muscle actin (α-SMA) and type I collagen (COL-1) in each group of cells were detected by Western blot, and the protein expression and localization of TfR1, Gpx4 in KFB were detected by immunofluorescence. GraphPad Prism 9.0 statistical software was used, and the measurement data were expressed as Mean±SD. Independent sample t-test was used for comparison between 2 groups, and one-way ANOVA was used for comparison between multiple groups, then LSD-t test was used for pairwise comparison between groups. P< 0.05 indicated that the differences were statistically significant. Results:The iron content and TfR1 protein expression were significantly higher in keloid compared with normal skin tissue ( P<0.01). The proliferation rate of KFB with different Erastin concentrations decreased gradually, the IC 50 was 0.61 μmol/L, and Fer-1 had no obvious toxicity to KFB in the range of 0.1~20 μmol/L. Scratch test showed that the migration rate of control group was significantly higher than that of NFB group ( P< 0.01) ; compared with the control group, KFB migration rate decreased significantly after Erastin intervention ( P<0.01) ; compared with the Erastin group, KFB migration was significantly accelerated in the Erastin+Fer-1 group ( P<0.01). Compared with the NFB group, ROS, MDA levels were significantly increased in the control group ( P< 0.01) ; compared with the control group, ROS, MDA levels and Fe 2+ content were significantly higher in the Erastin group ( P<0.01), while ROS, MDA levels and Fe 2+ content were significantly lower in the Fer-1 group ( P<0.01) ; compared with the Erastin group, MDA, ROS levels and Fe 2+content in the Erastin+ Fer-1 group were significantly decreased ( P<0.01). Western Blot showed that, compared with the NFB group, iron death indexes of SLC7A11 and GPx4 protein expression were significantly reduced ( P<0.01 or P<0.05), TfR1 protein expression was increased ( P<0.01), and fibrosis indexes of α-SMA and COL-1 protein expression were significantly increased ( P<0.01) in the control group; compared with the control group, SLC7A11 expression was reduced ( P<0.01) and TfR1, COL-1 expression increased ( P<0.01), while SLC7A11, GPx4 expression increased ( P< 0.01) and TfR1, α-SMA, COL-1 expression significantly decreased ( P<0.01) in the Fer-1 group; compared with the Erastin group, the GPx4, SLC7A11 expression was increased ( P< 0.01) and TfR1, α-SMA, COL-1 expression was significantly decreased ( P< 0.01) in the Erastin+Fer-1 group, suggesting that Fer-1 was able to reverse Erastin-induced ferroptosis and pro-fibrotic effects in KFB. Immunofluorescence showed that GPx4 was expressed in both nucleus and cytoplasm. Compared with control group, Fer-1 increased the fluorescence intensity of GPx4 in KFB ( P<0.01). Compared with Erastin group, the fluorescence intensity of GPx4 in Erastin+ Fer-1 group was significantly increased ( P<0.01). TfR1 was mainly expressed in cytoplasm. Compared with control group, Erastin increased the fluorescence intensity of TfR1 in KFB ( P< 0.05), while Fer-1 group significantly decreased it ( P < 0.01). Compared with Erastin group, the fluorescence intensity of TfR1 in Erastin+Fer-1 group was significantly reduced ( P<0.01). Conclusions:Iron overload and free iron increase in keloids. Erastin induces ferroptosis in KFB and aggravates keloid fibrosis. Fer-1 reverses the oxidative damage and iron accumulation induced by Erastin and effectively inhibits ferroptosis and keloid fibrosis in KFB.

Nuclear factor E2-related factor 2 (Nrf2) is a major regulator of redox homeostasis in cells, and Nrf2 signaling pathway has anti-inflammatory, anti-oxidative stress, and anti-fibrosis effects and plays an important role in wound healing and pathological scar formation and progression. This article reviewed the related research on the effect of oxidative stress and Nrf2 signaling pathway on pathological scars, and expounded the relationship between Nrf2 signaling pathway, oxidative stress and pathological scars, providing a new perspective for the mechanism study and clinical prevention and treatment of pathological scars.

Objective:To investigate the iron content and transferrin receptor 1 (TfR1) expression levels in keloid and normal skin tissues. Erastin induced ferroptosis model of keloid fibroblasts (KFB) is constructed in vitro, and the effects of Erastin and Ferrostatin-1 (Fer-1) on cell viability, ferrous ion (Fe 2+ ) content and lipid peroxidation, ferroptosis and fibrosis-related regulatory factors are examined. Methods:Six keloid tissues and six prepuces were collected from the First Affiliated Hospital of Xinjiang Medical University from March to June 2022. The tissue iron content kit was used to determine the iron content in the dermis, and TfR1 protein expression level was detected by Western blotting. Primary KFB and normal skin fibroblasts (NFB) were obtained by tissue cultivation, Erastin-induced KFB ferroptosis model and CCK-8 assay were used to detect the effects of different concentrations of Erastin and Fer-1 on cell viability, and to screen the appropriate drug concentration. The subsequent experiments were divided into five groups: NFB group, control group, Erastin (0.6 μmol/L) group, Fer-1 (1 μmol/L) group, and Erastin (0.6 μmol/L) + Fer-1 (1 μmol/L) group. KFB was used in the last 4 groups. Cell migration ability was detected by scratch assay. The contents of malondialdehyde (MDA), reactive oxygen species (ROS) and Fe 2+ were detected by fluorescence probe and kits; the protein expression levels of TfR1, glutathione peroxidase 4 (GPx4), solute carrier family 7 member 11 (SLC7A11), α-smooth muscle actin (α-SMA) and type I collagen (COL-1) in each group of cells were detected by Western blotting; the protein expression and localization of TfR1 and Gpx4 in KFB were detected by immunofluorescence staining. GraphPad Prism 9.0 statistical software was used in the statistical analyses, and the measurement data were expressed as Mean±SD. Independent samples t-test was used for comparison between 2 groups, and one-way ANOVA was used for comparison between multiple groups, LSD- t test was used for pairwise comparison between groups. P<0.05 indicated statistical significance. Results:The iron content and TfR1 protein expression level were significantly higher in keloids compared with normal skin tissue ( P<0.01). The proliferation rate of KFB decreased as the Erastin concentration increased, the IC 50 was 0.61 μmol/L, and Fer-1 had no obvious toxicity to KFB in the range of 0.1-20 μmol/L. Scratch test showed that the migration rate of control group was significantly higher than that of NFB group ( P<0.01); compared with the control group, KFB migration rate decreased significantly after Erastin intervention ( P<0.01); compared with the Erastin group, KFB migration was significantly accelerated in the Erastin+ Fer-1 group ( P<0.01). Compared with the NFB group, ROS, MDA levels were significantly increased in the control group ( P<0.01); compared with the control group, ROS, MDA levels and Fe 2+ content were significantly higher in the Erastin group ( P<0.01), while ROS, MDA levels and Fe 2+ content were significantly lower in the Fer-1 group ( P<0.05); compared with the Erastin group, MDA, ROS levels and Fe 2+ content in the Erastin+ Fer-1 group were significantly decreased ( P<0.01). Western blotting results showed that, compared with the NFB group, ferroptosis indexes of SLC7A11 and GPx4 protein expression levels were significantly reduced ( P<0.01), TfR1 protein expression was increased ( P<0.01), and protein expression of fibrosis indexes, α-SMA and COL-1 were significantly increased ( P<0.01) in the control group; compared with the control group, Erastin group had reduced SLC7A11 expression ( P<0.01) and increased TfR1, COL-1 expression ( P<0.01), while SLC7A11, GPx4 expression increased ( P<0.01) and TfR1, α-SMA, COL-1 decreased ( P<0.01) in the Fer-1 group; compared with the Erastin group, the GPx4 and SLC7A11 expression levels were increased ( P<0.01) and TfR1, α-SMA, COL-1 expression levels were significantly decreased ( P<0.01) in the Erastin+ Fer-1 group, suggesting that Fer-1 was able to reverse the Erastin-induced ferroptosis and pro-fibrotic effects in KFB. Immunofluorescence staining showed that GPx4 was expressed in both the nucleus and the cytoplasm. Compared with the control group, Fer-1 increased the fluorescence intensity of GPx4 in KFB ( P<0.01). Compared with the Erastin group, the fluorescence intensity of GPx4 in Erastin+ Fer-1 group was significantly increased ( P<0.01). TfR1 was mainly expressed in the cytoplasm. Compared with the control group, Erastin increased the fluorescence intensity of TfR1 in KFB ( P<0.05), while Fer-1 group significantly decreased it ( P<0.01). Compared with Erastin group, the fluorescence intensity of TfR1 in Erastin+ Fer-1 group was significantly reduced ( P<0.01). Conclusion:Iron overload is present in keloids and the free iron level is increased. Erastin is able to induce ferroptosis in KFB and aggravate keloid fibrosis. Fer-1 can reverse the oxidative damage and iron accumulation induced by Erastin, and is able to effectively inhibit ferroptosis and keloid fibrosis in KFB.

Objective:To understand the iron content and transferrin receptor 1 (TfR1) expression levels in keloid and normal skin tissues, an in vitro model of keloid fibroblasts (KFB) ferroptosis induced by Erastin was constructed, and the effects of Erastin and Ferrostatin-1(Fer-1) on cell viability, ferrous ion (Fe 2+) content and lipid peroxidation, ferroptosis and fibrosis-related regulatory factors were examined. Methods:Six keloid tissues and six normal skin tissues were collected from the First Affiliated Hospital of Xinjiang Medical University from March to June 2022, and the tissue iron content kit was used to determine the iron content in the dermis of the two tissues, and TfR1 protein expression was detected in the two tissues by Western blot. Primary KFB and normal skin fibroblasts (NFB) were obtained by tissue block culture method, and the effect of different concentrations of Erastin and Fer-1 on cell activity was detected by using Erastin-induced KFB ferroptosis model and CCK-8 method to screen the appropriate drug concentration. The follow-up experiments were divided into five groups: NFB group, control group, Erastin (0.6 μmol/L) group, Fer-1 (1 μmol/L) group, and Erastin (0.6 μmol/L) +Fer-1 (1 μmol/L) group, while KFB was used as the experimental object in the last 4 groups. Cell migration ability was detected by scratch assay, and malondialdehyde (MDA), reactive oxygen species (ROS) and Fe 2+ content in each group of cells were detected by fluorescent probe method and kits; the protein expression of TfR1, glutathione peroxidase 4 (GPx4), solute carrier family 7 member 11 (SLC7A11), α-smooth muscle actin (α-SMA) and type I collagen (COL-1) in each group of cells were detected by Western blot, and the protein expression and localization of TfR1, Gpx4 in KFB were detected by immunofluorescence. GraphPad Prism 9.0 statistical software was used, and the measurement data were expressed as Mean±SD. Independent sample t-test was used for comparison between 2 groups, and one-way ANOVA was used for comparison between multiple groups, then LSD-t test was used for pairwise comparison between groups. P< 0.05 indicated that the differences were statistically significant. Results:The iron content and TfR1 protein expression were significantly higher in keloid compared with normal skin tissue ( P<0.01). The proliferation rate of KFB with different Erastin concentrations decreased gradually, the IC 50 was 0.61 μmol/L, and Fer-1 had no obvious toxicity to KFB in the range of 0.1~20 μmol/L. Scratch test showed that the migration rate of control group was significantly higher than that of NFB group ( P< 0.01) ; compared with the control group, KFB migration rate decreased significantly after Erastin intervention ( P<0.01) ; compared with the Erastin group, KFB migration was significantly accelerated in the Erastin+Fer-1 group ( P<0.01). Compared with the NFB group, ROS, MDA levels were significantly increased in the control group ( P< 0.01) ; compared with the control group, ROS, MDA levels and Fe 2+ content were significantly higher in the Erastin group ( P<0.01), while ROS, MDA levels and Fe 2+ content were significantly lower in the Fer-1 group ( P<0.01) ; compared with the Erastin group, MDA, ROS levels and Fe 2+content in the Erastin+ Fer-1 group were significantly decreased ( P<0.01). Western Blot showed that, compared with the NFB group, iron death indexes of SLC7A11 and GPx4 protein expression were significantly reduced ( P<0.01 or P<0.05), TfR1 protein expression was increased ( P<0.01), and fibrosis indexes of α-SMA and COL-1 protein expression were significantly increased ( P<0.01) in the control group; compared with the control group, SLC7A11 expression was reduced ( P<0.01) and TfR1, COL-1 expression increased ( P<0.01), while SLC7A11, GPx4 expression increased ( P< 0.01) and TfR1, α-SMA, COL-1 expression significantly decreased ( P<0.01) in the Fer-1 group; compared with the Erastin group, the GPx4, SLC7A11 expression was increased ( P< 0.01) and TfR1, α-SMA, COL-1 expression was significantly decreased ( P< 0.01) in the Erastin+Fer-1 group, suggesting that Fer-1 was able to reverse Erastin-induced ferroptosis and pro-fibrotic effects in KFB. Immunofluorescence showed that GPx4 was expressed in both nucleus and cytoplasm. Compared with control group, Fer-1 increased the fluorescence intensity of GPx4 in KFB ( P<0.01). Compared with Erastin group, the fluorescence intensity of GPx4 in Erastin+ Fer-1 group was significantly increased ( P<0.01). TfR1 was mainly expressed in cytoplasm. Compared with control group, Erastin increased the fluorescence intensity of TfR1 in KFB ( P< 0.05), while Fer-1 group significantly decreased it ( P < 0.01). Compared with Erastin group, the fluorescence intensity of TfR1 in Erastin+Fer-1 group was significantly reduced ( P<0.01). Conclusions:Iron overload and free iron increase in keloids. Erastin induces ferroptosis in KFB and aggravates keloid fibrosis. Fer-1 reverses the oxidative damage and iron accumulation induced by Erastin and effectively inhibits ferroptosis and keloid fibrosis in KFB.

Nuclear factor E2-related factor 2 (Nrf2) is a major regulator of redox homeostasis in cells, and Nrf2 signaling pathway has anti-inflammatory, anti-oxidative stress, and anti-fibrosis effects and plays an important role in wound healing and pathological scar formation and progression. This article reviewed the related research on the effect of oxidative stress and Nrf2 signaling pathway on pathological scars, and expounded the relationship between Nrf2 signaling pathway, oxidative stress and pathological scars, providing a new perspective for the mechanism study and clinical prevention and treatment of pathological scars.

Objective:To investigate the iron content and transferrin receptor 1 (TfR1) expression levels in keloid and normal skin tissues. Erastin induced ferroptosis model of keloid fibroblasts (KFB) is constructed in vitro, and the effects of Erastin and Ferrostatin-1 (Fer-1) on cell viability, ferrous ion (Fe 2+ ) content and lipid peroxidation, ferroptosis and fibrosis-related regulatory factors are examined. Methods:Six keloid tissues and six prepuces were collected from the First Affiliated Hospital of Xinjiang Medical University from March to June 2022. The tissue iron content kit was used to determine the iron content in the dermis, and TfR1 protein expression level was detected by Western blotting. Primary KFB and normal skin fibroblasts (NFB) were obtained by tissue cultivation, Erastin-induced KFB ferroptosis model and CCK-8 assay were used to detect the effects of different concentrations of Erastin and Fer-1 on cell viability, and to screen the appropriate drug concentration. The subsequent experiments were divided into five groups: NFB group, control group, Erastin (0.6 μmol/L) group, Fer-1 (1 μmol/L) group, and Erastin (0.6 μmol/L) + Fer-1 (1 μmol/L) group. KFB was used in the last 4 groups. Cell migration ability was detected by scratch assay. The contents of malondialdehyde (MDA), reactive oxygen species (ROS) and Fe 2+ were detected by fluorescence probe and kits; the protein expression levels of TfR1, glutathione peroxidase 4 (GPx4), solute carrier family 7 member 11 (SLC7A11), α-smooth muscle actin (α-SMA) and type I collagen (COL-1) in each group of cells were detected by Western blotting; the protein expression and localization of TfR1 and Gpx4 in KFB were detected by immunofluorescence staining. GraphPad Prism 9.0 statistical software was used in the statistical analyses, and the measurement data were expressed as Mean±SD. Independent samples t-test was used for comparison between 2 groups, and one-way ANOVA was used for comparison between multiple groups, LSD- t test was used for pairwise comparison between groups. P<0.05 indicated statistical significance. Results:The iron content and TfR1 protein expression level were significantly higher in keloids compared with normal skin tissue ( P<0.01). The proliferation rate of KFB decreased as the Erastin concentration increased, the IC 50 was 0.61 μmol/L, and Fer-1 had no obvious toxicity to KFB in the range of 0.1-20 μmol/L. Scratch test showed that the migration rate of control group was significantly higher than that of NFB group ( P<0.01); compared with the control group, KFB migration rate decreased significantly after Erastin intervention ( P<0.01); compared with the Erastin group, KFB migration was significantly accelerated in the Erastin+ Fer-1 group ( P<0.01). Compared with the NFB group, ROS, MDA levels were significantly increased in the control group ( P<0.01); compared with the control group, ROS, MDA levels and Fe 2+ content were significantly higher in the Erastin group ( P<0.01), while ROS, MDA levels and Fe 2+ content were significantly lower in the Fer-1 group ( P<0.05); compared with the Erastin group, MDA, ROS levels and Fe 2+ content in the Erastin+ Fer-1 group were significantly decreased ( P<0.01). Western blotting results showed that, compared with the NFB group, ferroptosis indexes of SLC7A11 and GPx4 protein expression levels were significantly reduced ( P<0.01), TfR1 protein expression was increased ( P<0.01), and protein expression of fibrosis indexes, α-SMA and COL-1 were significantly increased ( P<0.01) in the control group; compared with the control group, Erastin group had reduced SLC7A11 expression ( P<0.01) and increased TfR1, COL-1 expression ( P<0.01), while SLC7A11, GPx4 expression increased ( P<0.01) and TfR1, α-SMA, COL-1 decreased ( P<0.01) in the Fer-1 group; compared with the Erastin group, the GPx4 and SLC7A11 expression levels were increased ( P<0.01) and TfR1, α-SMA, COL-1 expression levels were significantly decreased ( P<0.01) in the Erastin+ Fer-1 group, suggesting that Fer-1 was able to reverse the Erastin-induced ferroptosis and pro-fibrotic effects in KFB. Immunofluorescence staining showed that GPx4 was expressed in both the nucleus and the cytoplasm. Compared with the control group, Fer-1 increased the fluorescence intensity of GPx4 in KFB ( P<0.01). Compared with the Erastin group, the fluorescence intensity of GPx4 in Erastin+ Fer-1 group was significantly increased ( P<0.01). TfR1 was mainly expressed in the cytoplasm. Compared with the control group, Erastin increased the fluorescence intensity of TfR1 in KFB ( P<0.05), while Fer-1 group significantly decreased it ( P<0.01). Compared with Erastin group, the fluorescence intensity of TfR1 in Erastin+ Fer-1 group was significantly reduced ( P<0.01). Conclusion:Iron overload is present in keloids and the free iron level is increased. Erastin is able to induce ferroptosis in KFB and aggravate keloid fibrosis. Fer-1 can reverse the oxidative damage and iron accumulation induced by Erastin, and is able to effectively inhibit ferroptosis and keloid fibrosis in KFB.