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Objective To explore the protective mechanisms of hydrogen-rich saline on renal ischemiareperfusion injury.Methods Mice were divided in to 3 groups:control (sham operation),ischemia-reperfusion (IR) and ischemia-reperfusion+ hydrogen-rich saline (HRS).Mice in IR+ HRS group were administrated HRS by intravenous injection 3days and 1min before operation and 4 times in the following 2hours after operation.Mice in control and IR group were administrated normal saline as the same volume and frequency with IR + HRS group.Mice were sacrificed 24 hours after operation,creatinine and urea nitrogen in serum were detected by biochemical analyzer,MDA and SOD level were detected by spectrophotometer,expression of Bcl-xl,Bcl2,Bak,Bax,Cleaved Caspase-3 proteins level were detected by western blot.Results Compared to IR group,creatinine,urea nitrogen,MDA level decreased significantly after HRS consumption.SOD enzyme activity increased significantly after HRS consumption.HRS treatment down-regulates expression of Bak,Bax and Cleaved Caspase-3 protein level,and up-regulates expression of Bcl2,and Bcl-xl protein level.Conclusion HRS eliminates ROS and elevates antioxidant activity in renal after IR,besides,HRS also regulate apoptosis signal pathway to protect IR injury in renal.
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Objective@#To explore the effect of hydrogen-rich saline on the CD4+ CD25+ Foxp3+ Treg cells in a guinea pig model of allergic rhinitis (AR) and investigate the underling anti-inflammatory mechanism.@*Methods@#Using random number table, eighteen guinea pigs were divided into three groups (control group/AR group/HRS group, n=6 of each group). AR guinea pig model was built with ovalbumin and aluminum. The guinea pigs were injected with hydrogen-rich saline (HRS group) for ten days after sensitation. And control group was injected with equal normal saline at the same time. Number of sneezes, degree of runny nose and nasal rubbing movements were scored. Peripheral blood eosinophil count was recorded. The content of interleukin 10(IL-10) and transforming growth factor β (TGF-β) in the serum were detected by enzyme-linked immunosorbent assay (ELISA). Immunohistochemical method was taken to detect IL-10 and TGF-β in nasal mucosa. The proportion of CD4+ CD25+ Foxp3+ T cells in the CD4+ T cells of spleen and peripheral blood were determined with flow cytometry. SPSS 17.0 software was used to analyze the data.@*Results@#There was significant difference in symptom scores among them. The scores of AR group preceded control group, and HRS could decrease the scores of AR ((6.29±1.79) vs (1.01±0.71), (4.50±0.84) vs (6.29±1.79), F=24.725, all P<0.05). The highest number of eosinophils in the peripheral blood belonged to control group, and the number of eosinophils were dramatically reduced after HRS administration ((0.41±0.05)×109/L vs (0.25±0.03 )×109/L, (0.32±0.03)×109/L vs (0.41±0.05)×109/L, F=70.05, all P<0.05). The content of IL-10 and TGF-β in control group is peak ((86.88±17.17) pg/ml, (598.28±72.70) pg/ml, respectively), and compared with AR group, HRS also increased the expression of IL-10 and TGF-β of peripheral blood ((72.54±11.75) pg/ml vs (53.49±10.07) pg/ml, (530.23±57.15) pg/ml vs (482.69±65.96) pg/ml, F value was 28.357, 14.128, respectively, all P<0.05). The proportion of CD4+ CD25+ Foxp3+ Treg cells in controls exceeded HRS group and AR group (1.81%±0.10%, 1.29%±0.74%, respectively), and HRS treatment increased the ratio of CD4+ CD25+ Foxp3+ Treg cells than AR group of peripheral blood ((1.50%±0.11%) vs (1.15%±0.11%), F=168.96, P<0.05). But there was no significant diferences in splene tissue ((1.01%±0.08%) vs (0.98%±0.09%), F=97.381, P>0.05).@*Conclusion@#Both the number and the cytokine secretion of CD4+ CD25+ Foxp3+ Treg cells are decreased in AR group, HRS may inhibit inflammatory response and ameliorate AR via improving the number and the cytokine secretion.
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Objective To investigate the therapeutic effect of hydrogen-rich saline on the rheological behavior of leukocytes in mesentery capillary of rats with high-voltage electrical burn .Methods 180 rats were randomly divided into four groups :burn injury plus normal saline group ,burn injury plus hydrogen-rich saline group ,sham plus normal saline group ,and burn injury plus papaver-ine group .The rats were received saline ,hydrogen-rich saline ,saline ,papaverine at different time points after scald respectively .The changes of rheological behavior of leukocytes in mesentery capillary of rats before and after the injury were investigated .Results The rheological behavior of leukocytes in mesentery capillary of the control group were observed no significant change (P>0 .05) . In experimental group the rolling white blood cell count ,the number of leukocyte adhesion ,the length of contact of leukocyte-endo-thelial cell at each phase after injury were higher than those at 15 min before injury (P<0 .05);leukocyte rolling speed after injury is lower than that before injury (P<0 .05) .In treatment group and positive control group ,the rolling white blood cell count ,the number of leukocyte adhesion ,the length of contact of leukocyte-endothelial cell at each phase after injury were higher than those at 15 min before injury (P<0 .05) ,but compared with the experimental group ,the increase range was lower (P<0 .05) .leukocyte rolling speed after injury is lower than that before injury (P<0 .05) ,and compared with the experimental group ,the reduction was lower (P<0 .05) .Conclusion The hydrogen-rich brine can effectively reduce the changes of rheological behavior of leukocytes in mesentery capillary of rats caused by high-voltage electrical burn ,and have a protective effect on rat mesenteric .
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Objective To investigate the effect of combining propofol with hydrogen on organ damage and inflammation of sepsis in cecal ligation and puncture (CLP) mice model.Methods One hundred and forty male C57BL/6 mice were randomly divided into groups (n = 28): sham group, CLP group, propofol group, H2 group, and propofol and H2 group. The sepsis was induced by CLP operation. Mice in sham group did the same operation with ligation and puncture. The mice of propofol group and propofol and H2 group were given 50 mg/kg propofol through tail vein at 1 hour and 6 hours after CLP and the mice of H2 group and propofol and H2 group were given 5 mL/kg H2-rich saline i.p. at 1 hour and 6 hours after CLP. The survival rates were observed during 7 days in twenty mice of each group. Inferior vena cava blood and part lung, liver and kidney tissue were collected for detection of the concentration of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and high mobility group box 1 (HMGB1) at 24 hours after CLP in the 40 animals left (eachn = 8). Then, the rest tissue of lung, liver and kidney tissue were harvested to test histopathology and histological score.Results The 1, 2, 3, 5, 7 days survival rate of septic mice were 80%, 40%, 20%, 10%, and 0%, respectively. The survival rate of animals increased significantly after propofol or hydrogen-rich treatment, and the combined treatment can further increase survival rate to 90%, 75%, 60%, 55%, and 55%, respectively. Compared with the sham group, inflammatory factors were significantly increased in blood and organ tissues, cell degeneration, necrosis, congestion and inflammatory cell infiltration in lung, liver and kidney, and tissues histological scores were significantly increased. The levels of inflammatory factors were reduced in blood and tissues, cell degeneration, necrosis, congestion and inflammatory cell infiltration were alleviated in lung, liver and kidney, and tissues histological scores were decreased after propofol or hydrogen-rich treatment compared with CLP group; these indicators were further improved in propofol and H2 group compared with propofol group or H2 group [2, 3, 5, 7-day survival rate: 75% vs. 60%, 65%; 60% vs. 50%, 50%; 55% vs. 45%, 40%; 55% vs. 40%, 40%; blood TNF-α (ng/L): 367±74 vs. 612±132, 588±117; blood IL-1β (ng/L): 321±68 vs. 502±95, 476±86; blood HMGB1 (μg/L): 4.6±0.9 vs. 7.0±1.4, 6.8±1.3; lung TNF-α(ng/g): 307±70 vs. 512±132, 488±102; lung IL-1β (ng/g): 367±77 vs. 571±108, 466±89; lung HMGB1 (μg/g):5.1±1.0 vs. 7.8±1.7, 7.1±1.5; liver TNF-α (ng/g): 247±57 vs. 431±112, 389±87; liver IL-1β (ng/g): 267±58 vs. 417±85, 399±76; liver HMGB1 (μg/g): 4.2±1.1 vs. 7.1±1.6, 6.6±1.2; kidney TNF-α (ng/g): 257±41 vs. 480±89, 448±82; kidney IL-1β (ng/g): 258±39 vs. 409±68, 411±66; kidney HMGB1 (μg/g): 3.9±0.7 vs. 6.8±1.2, 5.7±1.0; histological scores: lung: 1.22±0.28 vs. 2.61±0.49, 2.58±0.44; liver: 1.38±0.32 vs. 2.76±0.51, 2.62±0.46; kidney: 1.19±0.25 vs. 2.43±0.41, 2.36±0.40; allP < 0.05].Conclusions Both propofol and H2 can improve the survival rate of sepsis, reduce tissue damage and the release of cytokines, and combined application of the two treatment was better.
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Objective To investigate the effect of hydrogen-rich saline on apoptosis in hippocampal neurons induced by cerebral ischemia-reperfusion in rats and PI3K/Akt/FoxO1 signaling pathway.Methods The rat model of focal cerebral ischemia-reperfusion was established by thread-occlusion of the middle cerebral artery in rats.SD rats were randomly divided into sham operation group (Sham group), ischemia-reperfusion group (I/R group) and hydrogen-rich saline treatment group (HRS group), 10 rats in each group.At 24 h after reperfusion, the serum levels of IL-6, TNF-a and IL-1β were detected by ELISA.Histological changes of the hippocampus were observed by pathology using HE staining.Apoptosis in brain tissues was observed by TUNEL staining.The expression changes of p-PI3K, Akt, caspase-3 and FoxO1 proteins were detected by Western blot assay.Results Compared with the sham group, pyramidal cells were arranged loosely in the I/R group and a large number of pyramidal cells were necrotized, and the amount of apoptotic hippocampal cells was increased.The levels of IL-1β, IL-6 and TNF-α were significantly increased (P< 0.05), as well as the expression of p-PI3K, Akt and caspase-3 in the brain tissue.However, the expression of FoxO1 protein was decreased.There were significant differences between the two groups (P< 0.05).Compared with the I/R group, the inflammatory factors were significantly decreased in the HRS group.The expressions of p-PI3K, Akt and caspase-3 were also significantly decreased, while the expression of FoxO1 protein was increased (P< 0.05).Conclusions Hydrogen-rich saline can reduce brain injury caused by ischemia-reperfusion, and its mechanism may be related to PI3K/Akt/FoxO1 signaling pathway.
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Objective To explore whether intravenous injection of hydrogen‐rich saline having the protective effect on sodium taurocholate induced severe acute pancreatitis(SAP) associated lung injury(APALI) in rats and its possible mechanisms .Methods Fifty‐four healthy male SD rats were randomly divided into sham‐operation group (Sham group) ,model group (SAP+ NS group) and hydrogen water treatment group (SAP + HRS group) ,and each group was subdivided into 6 ,12 ,24 h subgroups .Six rats were killed at each time point for collecting serum ,lung tissue and pancreas tissue .Serum TNF‐αand IL‐1βlevels ,lung wet /dry weight ratio ,expression of TNF‐αmRNA and IL‐1βmRNA in the lung tissue were detected .The pathological evaluation of pancreas and lung tissue injury was performed .Results (1)The levels of TNF‐α and IL‐1β in serum ,pancreas and lung tissue pathological scores ,TNF‐αmRNA and IL‐1βmRNA expression levels in the lung tissue and lung wet dry weight ratio at the time points of 6 , 12 ,24 h in the SAP+NS group and the SAP+ HRS group were higher than those in the sham group (P<0 .05) .(2) Compared with the SAP+NS group ,the levels of serum TNF‐α,TNF‐αmRNA expression level in the lung tissue and lung wet dry weight ra‐tio at all time points in the SAP+ HRS group were lower(P<0 .05);the levels of serum IL‐1β,pancreas and lung tissue pathologi‐cal score and IL‐1β‐mRNA expression at 6 h in the lung tissue had no statistical difference between the SAP+NS group and SAP+HRS group ,but which at time points of 12 ,24 h in the SAP+ HRS group were lower than those in the SAP+NS group(P<0 .05) . Conclusion HRS realize the protection on APALI possibly via its elective anti‐oxidation action for inhibiting oxidative stress injury related cytokines expression .
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The oxidative stress, inflammatory cytokines and apoptosis have been strongly implicated in the pathogenesis of multiple diseases. Recently, more and more research findings have demonstrated that hydrogen-rich saline (HRS) has the anti-oxidant, anti-inflammatory and anti-apoptotic effects in vivo and in vitro, and can be used to treat multiple diseases, such as ischemia/reperfusion injury, stroke, neurodegeneration, sepsis, neuropathic pain and multiple organ dysfunction syn-drome diseases. This article reviews the possible mechanism of HRS for the treatment of diseases.
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Objective To investigate the protective effect of hydrogen-rich saline on lung injury associated with severe acute pancreatitis and its impact on P38MAPK and NF-κB expressions.Methods Fifty-four male Wistar rats were randomly (random number) divided into three groups:(1) hydrogen-rich saline treatment group (HRS group,n =18),in which the rats were treated with hydrogen-rich saline (6 mL/kg) administered intravenously via tail vein and HRS (20 mL/kg) administered subcutaneously at 5 min after successful modeling.(2) Severe acute pancreatitis model group (SAP group,n =18),in which rats received equivalent volume of normal saline instead of hydrogen-rich saline both intravenously and subcutaneously as in HRS group.(3) Sham operation group (SO group,n =18),in which rats were treated with sham surgery,and received equivalent volume of normal saline as in SAP group.The model of severe acute pancreatitis (SAP) was made by retrograde injection of 5％ sodium taurocholate (1 mL/kg) into cholepancreatic duct.All rats were sacrificed at 3 h,12 h,and 24 h separately after the operation (n =6 at a time).The levels of serum amylase,lipase were measured.The ratio of wet and dry lung tissues was measured.The histopathological changes of lung tissues were observed under optic microscope.The expressions of P38MAPK,p-P38MAPK and NF-κB were measured by using immunohistochemistry method.Results Compared with SAP group,there were no significant differences in levels of serum amylase [12 h (5306.7±909) vs.(5435.0 ±441.2)] and lipase [12 h (1897.8 ±149.4) vs.(1917.9± 106.8)] in HRS group (P ＞0.05),but there were significant differences in the ratio of wet and dry lung tissues [12 h (3.12 ± 0.58) vs.(1.87 ± 0.25)] and histopathology scores [12 h (2.14 ± 0.38) vs.(3.58 ±0.32)] (P ＜0.05).There was no significant difference in expression of P38MAPK in lung tissues among three groups at 12 h.Compared with SO group,the expressions of p-P38MAPK and NF-κB were significant increased in SAP group at 12 h,however,they were lower significantly in HRS group than those in SAP group.Conclusions Hydrogen-rich saline has a protective effect on lung injury associated with severe acute pancreatitis,and its mechanism may be likely related to the antioxidant effect and inhibiting the activation of P38MAPK and NF-κB.
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Objective To study the effects of hydrogen-rich saline (HS) on the protection of hepatic injury induced by ischemia-reperfusion (I/R) in rats.Methods Male Sprague-Dawley rats (n =60) were randomly divided into three experimental groups:sham-operated group,I/R plus saline treatment group,and I/R plus hydrogen-rich saline treatment group.Reperfusion liver was conducted 180 mins after liver ischemia.Blood samples and liver tissues were collected.Result Serum ALT,AST levels,and MDA content,HMGB1,TNF-α,IL-1β and IL-6 levels in liver tissue were increased,but SOD and GSH activity were decreased significantly by I/R.Hydrogen-rich saline reduced oxidative stress and inflammatory reaction,and relieved morphological liver injury (P ＜ 0.01).Conclusion Hydrogen-rich saline attenuated I/R induced liver damage by reduction of oxidative injury and inflammatory reaction.
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Objective:To study the effect of hydrogen-rich saline on the prevention of liver mitochondrial injury induced by isch-emia-reperfusion (I/R) in rats. Methods:Male Sprague-Dawley rats (n=42) were randomly divided into three experimental groups (n=14), namely, sham-operated, I/R plus saline-treated (5 mL/kg, i.p.), and I/R plus hydrogen-rich saline-treated (5 mL/kg, i.p.) groups. Mi-tochondrial oxidative stress and functions, as well as morphologic changes in the mitochondria, were detected 180 min after reperfu-sion. Results:After I/R, mitochondrial swelling and vague cristae were observed. Mitochondrial functions were significantly decreased, but mitochondrial MDA and GSSH contents were increased by I/R. Hydrogen-rich saline reduced these markers, improved mitochondri-al ATP content and respiratory function, and relieved morphological mitochondrial injury (P<0.01). Conclusion:Hydrogen-rich saline attenuated I/R-induced liver mitochondrial damage and reduced mitochondrial oxidative stress.
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Objective To study the protective effect of hydrogen-rich saline (HRS) on apoptosis in skin flap after ischemia/reperfusion injury.Methods Total 18 Sprague-Dawley rats were randomly divided into three groups:a HRS treated group and two physiological saline treated groups (controls 1,2).The rats were anesthetized and an extended abdominal skin flap (6 cm × 9 cm) was elevated in each animal.Ischemia was induced by clamping the left right pedicle for 3 h,then HRS was administered intraperitoneally 10 min before reperfusion,and physiological saline was injected in control groups 1 and 2.In the control group 2,the flaps were elevated without occluding the artery and vein.Five days postoperation,apoptosis,TNF-α level in flap were measured with ELISA,NF-κB in nucleus was determined by Westernblot.Results Apoptotic rate represented (39.72±8.09) ％in HRS group and (69.43±13.27) ％ in control group 1,respectively.Treatment with HRS resulted in a marked reduction in apoptotic rate.TNF-α level was (516.408±38.674) pg/ml in the control group 1,a significant reduced TNF-α was measured in HRS group,accounting for (269.136 ±24.530) pg/ml.Moreover,NF-κB activation was significantly down-regulated by HRS.In control group 2,no significant apoptosis was observed because of non-blood occlusion,and there was no marked elevation of TNF-α and NF-κB.Conclusions HRS can protect skin from ischemia/reperfusion injury,attenuate apoptosis in flaps,which may be associated with the inhibition of TNF-α and NF-kb elevation.