BACKGROUND Diabetic foot ulcers(DFU),as severe complications of diabetes mellitus(DM),significantly compromise patient health and carry risks of amputation and mortality.AIM To offer new insights into the occurrence a...BACKGROUND Diabetic foot ulcers(DFU),as severe complications of diabetes mellitus(DM),significantly compromise patient health and carry risks of amputation and mortality.AIM To offer new insights into the occurrence and development of DFU,focusing on the therapeutic mechanisms of X-Paste(XP)of wound healing in diabetic mice.METHODS Employing traditional Chinese medicine ointment preparation methods,XP combines various medicinal ingredients.High-performance liquid chromatography(HPLC)identified XP’s main components.Using streptozotocin(STZ)-induced diabetic,we aimed to investigate whether XP participated in the process of diabetic wound healing.RNA-sequencing analyzed gene expression differences between XP-treated and control groups.Molecular docking clarified XP’s treatment mechanisms for diabetic wound healing.Human umbilical vein endothelial cells(HUVECs)were used to investigate the effects of Andrographolide(Andro)on cell viability,reactive oxygen species generation,apoptosis,proliferation,and metastasis in vitro following exposure to high glucose(HG),while NF-E2-related factor-2(Nrf2)knockdown elucidated Andro’s molecular mechanisms.RESULTS XP notably enhanced wound healing in mice,expediting the healing process.RNA-sequencing revealed Nrf2 upregulation in DM tissues following XP treatment.HPLC identified 21 primary XP components,with Andro exhibiting strong Nrf2 binding.Andro mitigated HG-induced HUVECs proliferation,metastasis,angiogenic injury,and inflammation inhibition.Andro alleviates HG-induced HUVECs damage through Nrf2/HO-1 pathway activation,with Nrf2 knockdown reducing Andro’s proliferative and endothelial protective effects.CONCLUSION XP significantly promotes wound healing in STZ-induced diabetic models.As XP’s key component,Andro activates the Nrf2/HO-1 signaling pathway,enhancing cell proliferation,tubule formation,and inflammation reduction.展开更多
Background:The aim of this study was to investigate the effects of different minimally invasive surgical procedures on intestinal muco-sal barrier function.Methods:In this study,76 patients who underwent minimally inv...Background:The aim of this study was to investigate the effects of different minimally invasive surgical procedures on intestinal muco-sal barrier function.Methods:In this study,76 patients who underwent minimally invasive gastric cancer surgery were selected,and peripheral blood was collected to test the levels of serum plasma D-lactic acid,diamine oxidase,and bacterial endotoxin before and 1 and 3 days after sur-gery.These markers were compared at different time points before and after surgery to understand the recovery of the intestinal muco-sal barrier function in patients after surgery.Results:On the first postoperative day,the change in serum D-lactic acid relative to the preoperative levels was significantly(P<0.05)lower in the laparoscopic surgery group(4.05[-0.195,6.917 mmol/L])than in the robot-assisted surgery group(7.56[5.190,12.145 mmol/L]).Both the serum D-lactic acid and bacterial endotoxin levels were significantly higher on the first postoperative day compared with preoperative levels,and although they showed a gradual decrease by the third day,they remained significantly higher than the pre-operative levels(P<0.05).The Student-Newman-Keuls method for pairwise comparison of the measurements at each time point dem-onstrated that the differences in D-lactic acid and bacterial endotoxin levels between the preoperative sample and the sample collected on the third postoperative day were statistically significant(P<0.05).Conclusions:Compared with the laparoscopic surgery group,the robotic surgery group showed larger changes in the postoperative serum D-lactic acid level,suggesting that the robotic surgery resulted in greater damage to the barrier function of the intestinal mucosa.The serum D-lactic acid and bacterial endotoxin levels were significantly higher in postoperative patients and showed a trend to gradually decrease,suggesting that the intestinal mucosal barrier function of patients after minimally invasive gastric cancer surgery is damaged and then gradually recovers.展开更多
BACKGROUND Diabetic skin ulcers,a significant global healthcare burden,are mainly caused by the inhibition of cell proliferation and impaired angiogenesis.XB130 is an adaptor protein that regulates cell proliferation ...BACKGROUND Diabetic skin ulcers,a significant global healthcare burden,are mainly caused by the inhibition of cell proliferation and impaired angiogenesis.XB130 is an adaptor protein that regulates cell proliferation and migration.However,the role of XB130 in the development of diabetic skin ulcers remains unclear.AIM To investigate whether XB130 can regulate the inhibition of proliferation and vascular damage induced by high glucose.Additionally,we aim to determine whether XB130 is involved in the healing process of diabetic skin ulcers,along with its molecular mechanisms.METHODS We conducted RNA-sequencing analysis to identify the key genes involved in diabetic skin ulcers.We investigated the effects of XB130 on wound healing using histological analyses.In addition,we used reverse transcription-quantitative polymerase chain reaction,Western blot,terminal deoxynucleotidyl transferasemediated dUTP nick end labeling staining,immunofluorescence,wound healing,and tubule formation experiments to investigate their effects on cellular processes in human umbilical vein endothelial cells(HUVECs)stimulated with high glucose.Finally,we performed functional analysis to elucidate the molecular mechanisms underlying diabetic skin ulcers.RESULTS RNA-sequencing analysis showed that the expression of XB130 was up-regulated in the tissues of diabetic skin ulcers.Knockdown of XB130 promoted the healing of skin wounds in mice,leading to an accelerated wound healing process and shortened wound healing time.At the cellular level,knockdown of XB130 alleviated high glucose-induced inhibition of cell proliferation and angiogenic impairment in HUVECs.Inhibition of the PI3K/Akt pathway removed the proliferative effects and endothelial protection mediated by XB130.CONCLUSION The findings of this study indicated that the expression of XB130 is up-regulated in high glucose-stimulated diabetic skin ulcers and HUVECs.Knockdown of XB130 promotes cell proliferation and angiogenesis via the PI3K/Akt signalling pathway,which accelerates the healing of diabetic skin ulcers.展开更多
基金Supported by the Shanghai Science and Technology Innovation Project,One Belt One Road International Joint Laboratory of Medical Mycology,No.21410750500。
文摘BACKGROUND Diabetic foot ulcers(DFU),as severe complications of diabetes mellitus(DM),significantly compromise patient health and carry risks of amputation and mortality.AIM To offer new insights into the occurrence and development of DFU,focusing on the therapeutic mechanisms of X-Paste(XP)of wound healing in diabetic mice.METHODS Employing traditional Chinese medicine ointment preparation methods,XP combines various medicinal ingredients.High-performance liquid chromatography(HPLC)identified XP’s main components.Using streptozotocin(STZ)-induced diabetic,we aimed to investigate whether XP participated in the process of diabetic wound healing.RNA-sequencing analyzed gene expression differences between XP-treated and control groups.Molecular docking clarified XP’s treatment mechanisms for diabetic wound healing.Human umbilical vein endothelial cells(HUVECs)were used to investigate the effects of Andrographolide(Andro)on cell viability,reactive oxygen species generation,apoptosis,proliferation,and metastasis in vitro following exposure to high glucose(HG),while NF-E2-related factor-2(Nrf2)knockdown elucidated Andro’s molecular mechanisms.RESULTS XP notably enhanced wound healing in mice,expediting the healing process.RNA-sequencing revealed Nrf2 upregulation in DM tissues following XP treatment.HPLC identified 21 primary XP components,with Andro exhibiting strong Nrf2 binding.Andro mitigated HG-induced HUVECs proliferation,metastasis,angiogenic injury,and inflammation inhibition.Andro alleviates HG-induced HUVECs damage through Nrf2/HO-1 pathway activation,with Nrf2 knockdown reducing Andro’s proliferative and endothelial protective effects.CONCLUSION XP significantly promotes wound healing in STZ-induced diabetic models.As XP’s key component,Andro activates the Nrf2/HO-1 signaling pathway,enhancing cell proliferation,tubule formation,and inflammation reduction.
基金funded by the Medical and Health Suitable Technology Development and Extension Project of Guangxi(No.S2021096)the Guangxi Key Laboratory of Enhanced Recovery After Surgery for Gastrointestinal Cancer.
文摘Background:The aim of this study was to investigate the effects of different minimally invasive surgical procedures on intestinal muco-sal barrier function.Methods:In this study,76 patients who underwent minimally invasive gastric cancer surgery were selected,and peripheral blood was collected to test the levels of serum plasma D-lactic acid,diamine oxidase,and bacterial endotoxin before and 1 and 3 days after sur-gery.These markers were compared at different time points before and after surgery to understand the recovery of the intestinal muco-sal barrier function in patients after surgery.Results:On the first postoperative day,the change in serum D-lactic acid relative to the preoperative levels was significantly(P<0.05)lower in the laparoscopic surgery group(4.05[-0.195,6.917 mmol/L])than in the robot-assisted surgery group(7.56[5.190,12.145 mmol/L]).Both the serum D-lactic acid and bacterial endotoxin levels were significantly higher on the first postoperative day compared with preoperative levels,and although they showed a gradual decrease by the third day,they remained significantly higher than the pre-operative levels(P<0.05).The Student-Newman-Keuls method for pairwise comparison of the measurements at each time point dem-onstrated that the differences in D-lactic acid and bacterial endotoxin levels between the preoperative sample and the sample collected on the third postoperative day were statistically significant(P<0.05).Conclusions:Compared with the laparoscopic surgery group,the robotic surgery group showed larger changes in the postoperative serum D-lactic acid level,suggesting that the robotic surgery resulted in greater damage to the barrier function of the intestinal mucosa.The serum D-lactic acid and bacterial endotoxin levels were significantly higher in postoperative patients and showed a trend to gradually decrease,suggesting that the intestinal mucosal barrier function of patients after minimally invasive gastric cancer surgery is damaged and then gradually recovers.
基金the National Natural Science Foundation of China,No.82272355Shanghai Science and Technology Committee,No.21410750500.
文摘BACKGROUND Diabetic skin ulcers,a significant global healthcare burden,are mainly caused by the inhibition of cell proliferation and impaired angiogenesis.XB130 is an adaptor protein that regulates cell proliferation and migration.However,the role of XB130 in the development of diabetic skin ulcers remains unclear.AIM To investigate whether XB130 can regulate the inhibition of proliferation and vascular damage induced by high glucose.Additionally,we aim to determine whether XB130 is involved in the healing process of diabetic skin ulcers,along with its molecular mechanisms.METHODS We conducted RNA-sequencing analysis to identify the key genes involved in diabetic skin ulcers.We investigated the effects of XB130 on wound healing using histological analyses.In addition,we used reverse transcription-quantitative polymerase chain reaction,Western blot,terminal deoxynucleotidyl transferasemediated dUTP nick end labeling staining,immunofluorescence,wound healing,and tubule formation experiments to investigate their effects on cellular processes in human umbilical vein endothelial cells(HUVECs)stimulated with high glucose.Finally,we performed functional analysis to elucidate the molecular mechanisms underlying diabetic skin ulcers.RESULTS RNA-sequencing analysis showed that the expression of XB130 was up-regulated in the tissues of diabetic skin ulcers.Knockdown of XB130 promoted the healing of skin wounds in mice,leading to an accelerated wound healing process and shortened wound healing time.At the cellular level,knockdown of XB130 alleviated high glucose-induced inhibition of cell proliferation and angiogenic impairment in HUVECs.Inhibition of the PI3K/Akt pathway removed the proliferative effects and endothelial protection mediated by XB130.CONCLUSION The findings of this study indicated that the expression of XB130 is up-regulated in high glucose-stimulated diabetic skin ulcers and HUVECs.Knockdown of XB130 promotes cell proliferation and angiogenesis via the PI3K/Akt signalling pathway,which accelerates the healing of diabetic skin ulcers.
