Hydrogen can relieve tissue-damaging oxidative stress, inflammation and apoptosis. Injection of hydrogen-rich saline is an effective method for transporting molecular hydrogen. We hypothesized that hydrogen-rich salin...Hydrogen can relieve tissue-damaging oxidative stress, inflammation and apoptosis. Injection of hydrogen-rich saline is an effective method for transporting molecular hydrogen. We hypothesized that hydrogen-rich saline would promote the repair of spinal cord injury induced by Allen＇s method in rats. At 0.5, 1, 2, 4, 8, 12 and 24 hours after injury, then once daily for 2 weeks, 0.25 mL/kg hydrogen-rich saline was infused into the subarachnoid space through a catheter. Results at 24 hours, 48 hours, 1 week and 2 weeks after injury showed that hydrogen-rich saline markedly reduced cell death, inflammatory cell infiltration, serum malondialdehyde content, and caspa se-3 immunoreactivity, elevated serum superoxide dismutase activity and calcitonin gene-related peptide immunoreactivity, and improved motor function in the hindlimb. The present study confirms that hydrogen-rich saline injected within 2 weeks of injury effectively contributes to the repair of spinal cord injury in the acute stage.展开更多
Objective: Skin damage induced by ischemia/reperfusion (I/R) is a multifactorial process that often occurs in plastic surgery. The mechanisms of I/R injury include hypoxia, inflammation, and oxidative damage. Hydrogen...Objective: Skin damage induced by ischemia/reperfusion (I/R) is a multifactorial process that often occurs in plastic surgery. The mechanisms of I/R injury include hypoxia, inflammation, and oxidative damage. Hydrogen gas has been reported to alleviate cerebral I/R injury by acting as a free radical scavenger. Here, we assessed the protective effect of hydrogen-rich saline (HRS) on skin flap I/R injury. Methods: Abdominal skin flaps of rats were elevated and ischemia was induced for 3 h; subsequently, HRS or physiological saline was administered intraperitoneally 10 min before reperfusion. On postoperative Day 5, flap survival, blood perfusion, the accumulation of reactive oxygen species (ROS), and levels of cytokines were evaluated. Histological examinations were performed to assess inflammatory cell infiltration. Results: Skin flap survival and blood flow perfusion were improved by HRS relative to the controls. The production of malondialdehyde (MDA), an indicator of lipid peroxidation, was markedly reduced. A multiplex cytokine assay revealed that HRS reduced the elevation in the levels of inflammatory cytokines, chemokines and growth factors, with the exception of RANTES (regulated on activation, normal T-cell expressed and secreted) growth factor. HRS treatment also reduced inflammatory cell infiltration induced by I/R injury. Conclusions: Our findings suggest that HRS mitigates I/R injury by decreasing inflammation and, therefore, has the potential for application as a therapy for improving skin flap survival.展开更多
Background: Hydrogen-rich saline(HRS) has antioxidative, anti-inflammatory and anti-apoptotic properties. We investigated the effects of hydrogen on hepatic ischemia-reperfusion(I/R) and laparoscopic hepatectomy in sw...Background: Hydrogen-rich saline(HRS) has antioxidative, anti-inflammatory and anti-apoptotic properties. We investigated the effects of hydrogen on hepatic ischemia-reperfusion(I/R) and laparoscopic hepatectomy in swine. Methods: Twenty-one healthy Bama miniature pigs were randomly divided into the sham group, ischemia-reperfusion injury(IRI) group, HRS-5(5 m L/kg) group, and HRS-10(10 m L/kg) group. HRS was injected through the portal vein 10 min before reperfusion and at postoperative day 1, 2 and 3. The roles of HRS on oxidative stress, inflammatory response and liver regeneration were studied. Results: Compared with the IRI group, HRS treatment attenuated oxidative stress by increasing catalase activity and reducing myeloperoxidase. White blood cells in the HRS-10 group were reduced compared with the IRI group( P < 0.01). In the HRS-10 group, interleukin-1 beta, interleukin-6 and tumor necrosis factor alpha, C-reactive protein and cortisol were downregulated, whereas interleukin-10 was upregulated. In addition, HRS attenuated endothelial cell injury and promoted the secretion of angiogenic cytokines, including vascular endothelial growth factor, angiopoietin-1 and angiopoietin-2. HRS elevated the levels of hepatocyte growth factor, Cyclin D1, proliferating cell nuclear antigen, Ki-67 and reduced the secretion of transforming growth factor-beta. Conclusions: HRS treatment may exert a protective effect against I/R and hepatectomy-induced hepatic damage by reducing oxidative stress, suppressing the inflammatory response and promoting liver regeneration.展开更多
Exposure of skin to solar ultraviolet（UV） radiation induces photo-damage.Ultraviolet B（UVB） is the major component of UV radiation which induces the production of reactive oxygen species（ROS） and plays an impor-...Exposure of skin to solar ultraviolet（UV） radiation induces photo-damage.Ultraviolet B（UVB） is the major component of UV radiation which induces the production of reactive oxygen species（ROS） and plays an impor-tant role in photo-damage.Hydrogen gas reduces ROS and alleviates inflammation.In this study,we sought to demonstrate that hydrogen-rich saline has the effect on skin injuries caused by UVB radiation.UVB radiation was irradiated on female C57BL/6 rats to induce skin injury.Hydrogen-rich saline and nitrogen-rich saline were ad-ministered to rats by intraperitoneal injection.Skin damage was detected by microscope after injury.UVB radia-tion had a significant affection in tumor necrosis factor alpha,interleukin（IL）-1β and IL-6 levels,tissue superox-ide dismutase,malondialdehyde and nitric oxide activity.Hydrogen-rich saline had a protective effect by altering the levels of these markers and relieved morphological skin injury.Hydrogen-rich saline protected against UVB radiation injury,possibly by reducing inflammation and oxidative stress.展开更多
AIM：To investigate the effects of hydrogen-rich saline（HRS）on microglia activation and Sirtuin type 1（Sirt1）in rats with N-methyl-N-nitrosourea（MNU）-induced retinitis pigmentosa（RP）.METHODS：Rats were divided...AIM：To investigate the effects of hydrogen-rich saline（HRS）on microglia activation and Sirtuin type 1（Sirt1）in rats with N-methyl-N-nitrosourea（MNU）-induced retinitis pigmentosa（RP）.METHODS：Rats were divided into norm（N）group,model（M）group and HRS（H）group.Rats in M and H groups were given saline and HRS respectively prior to and after administration of MNU.At one day（d1）and d3 afterwards,electroretinogram and histological examination were performed to confirm the effects of HRS on retinal function and structure of MNU-induced RP.Immunofluorescence staining of anti-ionized calcium-binding adapter molecule 1（Iba1）,a maker of microglia cells,was performed,with quantitative real-time polymerase chain reaction（qRT-PCR）for its m RNA quantification.Moreover,Sirt1 m RNA and protein expression in the retinas were detected by Western blot and qRT-PCR.RESULTS：HRS preserved the retinal function and mitigated the reduction of photoreceptor degeneration in MNU-treated retinas.The presence of microglia cells was somewhat more obvious in H group than that in M group at d1.HRS suppressed the further activation of microglia cells,with the number of microglia cells less than that of M group at d3.Results of qRT-PCR of Iba1 were consistent with those of immunofluorescence staining,with the m RNA expression of Iba1 in H group more intensive than that of M group at d1（P〈0.05）,while less than that of M group at d3（P〈0.05）.Furthermore,the Sirt1 m RNA and protein expression decreased after MNU administration,while HRS mitigated the MNU-induced downregulation of Sirt1.CONCLUSION：HRS can effectively keep microglia activation induced by MNU to an appropriate extent,while upregulate Sirt1 in MNU-induced RP.展开更多
基金supported by a grant from Hunan Provincial Science and Technology Ministry of China,No.2015JJ6116
文摘Hydrogen can relieve tissue-damaging oxidative stress, inflammation and apoptosis. Injection of hydrogen-rich saline is an effective method for transporting molecular hydrogen. We hypothesized that hydrogen-rich saline would promote the repair of spinal cord injury induced by Allen＇s method in rats. At 0.5, 1, 2, 4, 8, 12 and 24 hours after injury, then once daily for 2 weeks, 0.25 mL/kg hydrogen-rich saline was infused into the subarachnoid space through a catheter. Results at 24 hours, 48 hours, 1 week and 2 weeks after injury showed that hydrogen-rich saline markedly reduced cell death, inflammatory cell infiltration, serum malondialdehyde content, and caspa se-3 immunoreactivity, elevated serum superoxide dismutase activity and calcitonin gene-related peptide immunoreactivity, and improved motor function in the hindlimb. The present study confirms that hydrogen-rich saline injected within 2 weeks of injury effectively contributes to the repair of spinal cord injury in the acute stage.
基金Project (No. 7132169) supported by the Beijing Natural Science Foundation, China
文摘Objective: Skin damage induced by ischemia/reperfusion (I/R) is a multifactorial process that often occurs in plastic surgery. The mechanisms of I/R injury include hypoxia, inflammation, and oxidative damage. Hydrogen gas has been reported to alleviate cerebral I/R injury by acting as a free radical scavenger. Here, we assessed the protective effect of hydrogen-rich saline (HRS) on skin flap I/R injury. Methods: Abdominal skin flaps of rats were elevated and ischemia was induced for 3 h; subsequently, HRS or physiological saline was administered intraperitoneally 10 min before reperfusion. On postoperative Day 5, flap survival, blood perfusion, the accumulation of reactive oxygen species (ROS), and levels of cytokines were evaluated. Histological examinations were performed to assess inflammatory cell infiltration. Results: Skin flap survival and blood flow perfusion were improved by HRS relative to the controls. The production of malondialdehyde (MDA), an indicator of lipid peroxidation, was markedly reduced. A multiplex cytokine assay revealed that HRS reduced the elevation in the levels of inflammatory cytokines, chemokines and growth factors, with the exception of RANTES (regulated on activation, normal T-cell expressed and secreted) growth factor. HRS treatment also reduced inflammatory cell infiltration induced by I/R injury. Conclusions: Our findings suggest that HRS mitigates I/R injury by decreasing inflammation and, therefore, has the potential for application as a therapy for improving skin flap survival.
基金supported by grants from the National Natural Science Foundation of China(31472245 and 31772807)
文摘Background: Hydrogen-rich saline(HRS) has antioxidative, anti-inflammatory and anti-apoptotic properties. We investigated the effects of hydrogen on hepatic ischemia-reperfusion(I/R) and laparoscopic hepatectomy in swine. Methods: Twenty-one healthy Bama miniature pigs were randomly divided into the sham group, ischemia-reperfusion injury(IRI) group, HRS-5(5 m L/kg) group, and HRS-10(10 m L/kg) group. HRS was injected through the portal vein 10 min before reperfusion and at postoperative day 1, 2 and 3. The roles of HRS on oxidative stress, inflammatory response and liver regeneration were studied. Results: Compared with the IRI group, HRS treatment attenuated oxidative stress by increasing catalase activity and reducing myeloperoxidase. White blood cells in the HRS-10 group were reduced compared with the IRI group( P < 0.01). In the HRS-10 group, interleukin-1 beta, interleukin-6 and tumor necrosis factor alpha, C-reactive protein and cortisol were downregulated, whereas interleukin-10 was upregulated. In addition, HRS attenuated endothelial cell injury and promoted the secretion of angiogenic cytokines, including vascular endothelial growth factor, angiopoietin-1 and angiopoietin-2. HRS elevated the levels of hepatocyte growth factor, Cyclin D1, proliferating cell nuclear antigen, Ki-67 and reduced the secretion of transforming growth factor-beta. Conclusions: HRS treatment may exert a protective effect against I/R and hepatectomy-induced hepatic damage by reducing oxidative stress, suppressing the inflammatory response and promoting liver regeneration.
文摘Exposure of skin to solar ultraviolet（UV） radiation induces photo-damage.Ultraviolet B（UVB） is the major component of UV radiation which induces the production of reactive oxygen species（ROS） and plays an impor-tant role in photo-damage.Hydrogen gas reduces ROS and alleviates inflammation.In this study,we sought to demonstrate that hydrogen-rich saline has the effect on skin injuries caused by UVB radiation.UVB radiation was irradiated on female C57BL/6 rats to induce skin injury.Hydrogen-rich saline and nitrogen-rich saline were ad-ministered to rats by intraperitoneal injection.Skin damage was detected by microscope after injury.UVB radia-tion had a significant affection in tumor necrosis factor alpha,interleukin（IL）-1β and IL-6 levels,tissue superox-ide dismutase,malondialdehyde and nitric oxide activity.Hydrogen-rich saline had a protective effect by altering the levels of these markers and relieved morphological skin injury.Hydrogen-rich saline protected against UVB radiation injury,possibly by reducing inflammation and oxidative stress.
基金Supported by the Natural Science Foundation of China(No.81300836)the Foundation of Open Sharing Platform of Science and Technology of Shaanxi Province,China(No.2015FWPT-02)
文摘AIM：To investigate the effects of hydrogen-rich saline（HRS）on microglia activation and Sirtuin type 1（Sirt1）in rats with N-methyl-N-nitrosourea（MNU）-induced retinitis pigmentosa（RP）.METHODS：Rats were divided into norm（N）group,model（M）group and HRS（H）group.Rats in M and H groups were given saline and HRS respectively prior to and after administration of MNU.At one day（d1）and d3 afterwards,electroretinogram and histological examination were performed to confirm the effects of HRS on retinal function and structure of MNU-induced RP.Immunofluorescence staining of anti-ionized calcium-binding adapter molecule 1（Iba1）,a maker of microglia cells,was performed,with quantitative real-time polymerase chain reaction（qRT-PCR）for its m RNA quantification.Moreover,Sirt1 m RNA and protein expression in the retinas were detected by Western blot and qRT-PCR.RESULTS：HRS preserved the retinal function and mitigated the reduction of photoreceptor degeneration in MNU-treated retinas.The presence of microglia cells was somewhat more obvious in H group than that in M group at d1.HRS suppressed the further activation of microglia cells,with the number of microglia cells less than that of M group at d3.Results of qRT-PCR of Iba1 were consistent with those of immunofluorescence staining,with the m RNA expression of Iba1 in H group more intensive than that of M group at d1（P〈0.05）,while less than that of M group at d3（P〈0.05）.Furthermore,the Sirt1 m RNA and protein expression decreased after MNU administration,while HRS mitigated the MNU-induced downregulation of Sirt1.CONCLUSION：HRS can effectively keep microglia activation induced by MNU to an appropriate extent,while upregulate Sirt1 in MNU-induced RP.
