RvD1 Attenuated Susceptibility to Ischemic AKI in Diabetes by Downregulating Nuclear Factor-κ B Signal and Inhibiting Apoptosis

BackgroundAcute kidney injury (AKI), when occurring in diabetic kidney disease (DKD), is known to be more severe and difficult to recover from. Inflammation and apoptosis may contribute to the heightened sensitivity of, and non-recovery from, AKI in patients with DKD. Resolvin D1 (RvD1) is a potent lipid mediator which can inhibit the inflammatory response and apoptosis in many diseases. However, it has been reported that the RvD1 levels were decreased in diabetes, which may explain why DKD is more susceptible to AKI.MethodsFor animal experiments, diabetic nephropathy (DN) mice were induced by streptozotocin (STZ) injection intraperitoneally. Renal ischemia–reperfusion was used to induce AKI. Blood urea nitrogen (BUN) and serum creatinine were determined using commercial kits to indicate renal function. Renal apoptosis was examined by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Real-time polymerase chain reaction (PCR) was used to detect the marker of inflammatory response. Western blot was used to detect the expression of nuclear factor-κB (NF-κB)-related proteins. For clinical study, 12 cases diagnosed with DKD were enrolled in this study, and an equal number of non-diabetic renal disease patients (NDKD) were recruited as a control group. The serum RvD1 in DKD or NDKD patients were detected through an ELISA kit.ResultsIn clinical study, we found that the serum RvD1 levels were decreased in DKD patients compared to those in NDKD patients. Decreased serum RvD1 levels were responsible for the susceptibility to ischemic AKI in DKD patients. In animal experiments, both the serum RvD1 and renal ALX levels were downregulated. RvD1 treatment could ameliorate renal function and histological damage after ischemic injury in DN mice. RvD1 treatment also could inhibit the inflammatory response. Di-tert-butyl dicarbonate (BOC-2) treatment could deteriorate renal function and histological damage after ischemic injury in non-diabetic mice. RvD1 could inhibit the NF-κB activation and suppress inflammatory response mainly by inhibiting NF-κB signaling.ConclusionRvD1 attenuated susceptibility to ischemic AKI in diabetes by downregulating NF-κB signaling and inhibiting apoptosis. Downregulated serum RvD1 levels could be the crucial factor for susceptibility to ischemic AKI in diabetes.

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Borate reduces experimental supra-celiac aortic clamping-induced oxidative stress in lung and kidney, but fails to prevent organ damage

Turkish Journal of Thoracic and Cardiovascular Surgery ◽

10.5606/tgkdc.dergisi.2021.21870 ◽

2021 ◽

Vol 29 (3) ◽

pp. 320-329

Author(s):

Tünay Kurtoğlu ◽

Selim Durmaz ◽

Ömer Faruk Rahman ◽

Nesibe Kahraman Çetin ◽

Mustafa Yılmaz ◽

...

Keyword(s):

Dimethyl Sulfoxide ◽

Ischemia Reperfusion ◽

Interleukin 1 ◽

Control Group ◽

Nuclear Factor ◽

Necrosis Factor Alpha ◽

Aortic Clamping ◽

Nuclear Factor Kappa ◽

Histological Damage ◽

Nuclear Factor Kappa Beta

Background: This study aims to investigate the effects of 2-aminoethoxydiphenyl borate (2-APB) on aortic clamping-induced lung and kidney tissue oxidation, tissue inflammation, and histological damage in a rat model. Methods: A total of 28 adult female Wistar albino rats were randomly allocated to four equal groups: Control group, ischemia-reperfusion group, dimethyl sulfoxide group, and 2-APB group. Animals in the control group underwent median laparotomy. In the remaining groups, supra-celiac aorta was clamped for 45 min and, then, reperfusion was constituted for 60 min. The 2-APB (2 mg/kg) was administered before clamping. The remaining groups received saline (ischemia-reperfusion group) or dimethyl sulfoxide (dimethyl sulfoxide group). Kidney and lung tissue samples were harvested at the end of reperfusion. Results: Aortic occlusion caused increased tissue total oxidant status and reduced total antioxidant status and glutathione levels in the ischemia-reperfusion and dimethyl sulfoxide groups. Tissue interleukin-1 beta and tumor necrosis factor-alpha levels, nuclear factor kappa beta activation, and histological damage severity scores were also higher in these groups. The 2-APB treatment eliminated the increase in total oxidant status and the decrease in total antioxidant status and glutathione levels. It also caused a decrease in the interleukin-1 beta levels, although it did not significantly alter the tumor necrosis factor-alpha levels, nuclear factor kappa beta immunoreactivity, and histological damage scores. Conclusion: Borate exerted a beneficial antioxidant effect as evidenced by reduced oxidative stress; however, it did not inhibit nuclear factor kappa beta activation and prevent histological damage in supra-celiac aortic clamping-induced kidney and lung injury in rats.

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Inhaled Nitric Oxide Attenuates Reperfusion Inflammatory Responses in Humans

Anesthesiology ◽

10.1097/00000542-200702000-00015 ◽

2007 ◽

Vol 106 (2) ◽

pp. 275-282 ◽

Cited By ~ 55

Author(s):

Mali Mathru ◽

Ruksana Huda ◽

Daneshvari R. Solanki ◽

Stephen Hays ◽

John D. Lang

Keyword(s):

Nitric Oxide ◽

Inflammatory Response ◽

Ischemia Reperfusion ◽

Inhaled Nitric Oxide ◽

Human Model ◽

Pulmonary Vasculature ◽

Nuclear Factor Kappab ◽

Control Group ◽

Nuclear Factor ◽

Nitrate And Nitrite

Background Reduced bioavailability of endothelium-derived nitric oxide associated with reperfusion could potentially exacerbate the inflammatory response during reperfusion. Evidence suggests the pharmacologic effects of inhaled nitric oxide may extend beyond the pulmonary vasculature, and this is attributed to nitric oxide-derived complexes in blood that ultimately orchestrate antiinflammatory effects. In this study, the authors evaluated the potential for inhaled nitric oxide (80 ppm) to attenuate inflammation instigated by ischemia-reperfusion in a human model using patients undergoing knee surgery where a tourniquet was used to produce a bloodless surgical field. Methods Inhaled nitric oxide (80 ppm) was administered before tourniquet application and continued throughout reperfusion until the completion of surgery. Venous blood samples were collected before and after reperfusion, for the measurements of nitrate and nitrite, CD11b/CD18, soluble P-selectin, and lipid hydroperoxide. Muscle biopsies were obtained from the quadriceps muscle before skin closure and analyzed for myeloperoxide, conjugated dienes, and nuclear factor-kappaB translocation. Results Administration of inhaled nitric oxide (80 ppm) significantly attenuated the inflammatory response characterized by reduced expression of CD11b/CD18, P-selectin, and nuclear factor kappaB compared with the control group. This was accompanied by increased plasma levels of nitrate and nitrite and reduced oxidative stress. Conclusions Administration of inhaled nitric oxide at 80 ppm significantly reduces inflammation in lower extremity ischemia-reperfusion in humans. This observation supports the concept that during diseases characterized by dysfunction in nitric oxide metabolism, inhaled nitric oxide may be an effective therapy to replenish systemic nitric oxide, thus retarding inflammatory-mediated injury.

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Abstract 138: Remote Ischemic Postconditioning Alleviates Postresuscitation Inflammatory Response and Pulmonary Edema in a Porcine Model of Cardiac Arrest

Circulation ◽

10.1161/circ.130.suppl_2.138 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Jiefeng Xu ◽

Sen Ye ◽

Zilong Li ◽

Moli Wang ◽

Zhengquan Wang ◽

...

Keyword(s):

Cardiac Arrest ◽

Inflammatory Response ◽

Pulmonary Edema ◽

Porcine Model ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Limb Ischemia ◽

Multiple Organ ◽

Control Group ◽

Lung Water

Introduction: Systemic ischemia-reperfusion injury produced by CA and resuscitation can result in severe post-cardiac arrest syndrome; which includes systemic inflammatory response and multiple organ dysfunction syndrome such as acute pulmonary edema. We previously demonstrated that remote ischemic post-conditioning (RIpostC) improved post-resuscitation myocardial and cerebral function in a rat model of CA. In this study, we investigated the effects of RIpostC on inflammatory response and pulmonary edema after CPR in a porcine model. Hypothesis: RIpostC would alleviate post-resuscitation inflammatory response and pulmonary edema in a porcine model of CA. Methods: Fourteen male domestic pigs weighing 37 ± 2 kg were utilized. Ventricular fibrillation was electrically induced and untreated for 10 mins. The animals were then randomized to receive RIpostC or control. Coincident with the start of CPR, RIpostC was induced by four cycles of 5 mins of limb ischemia and then 5 mins of reperfusion. Defibrillation was attempted after 5 mins of CPR. The resuscitated animals were monitored for 4 hrs and observed for an additional 68 hrs. Results: Six of the seven animals in each group were successfully resuscitated. After resuscitation, significantly lower levels of tumor necrosis factor-α and interleukin-6 were measured in the animals that received RIpostC when compared with the control group. Post-resuscitation extra-vascular lung water index was lower in the RIpostC group than in the control group; in which the differences were significant at 2,3 and 4 hrs (Table). Conclusion: In a porcine model of CA, RIpostC significantly alleviates post-resuscitation inflammatory response and pulmonary edema.

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Local anesthetics worsen renal function after ischemia-reperfusion injury in rats

AJP Renal Physiology ◽

10.1152/ajprenal.00108.2003 ◽

2004 ◽

Vol 286 (1) ◽

pp. F111-F119 ◽

Cited By ~ 18

Author(s):

H. Thomas Lee ◽

Igor E. Krichevsky ◽

Hua Xu ◽

Ayuko Ota-Setlik ◽

Vivette D. D'Agati ◽

...

Keyword(s):

Cell Death ◽

Renal Function ◽

Renal Dysfunction ◽

Local Anesthetic ◽

Local Anesthetics ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Terminal Deoxynucleotidyl Transferase ◽

Morphological Identification ◽

Sham Operation

Local anesthetics are widely used during the perioperative period, even in patients with preexisting renal disease. However, local anesthestics have been shown to cause cell death in multiple cell lines, including human kidney proximal tubule cells. We questioned whether local anesthetics potentiate renal dysfunction after ischemia-reperfusion (I/R) injury in vivo. Rats were implanted with subcutaneous miniosmotic pumps that continuously delivered lidocaine (2 mg·kg-1·h-1), bupivacaine (0.4 mg·kg-1·h-1), tetracaine (1 mg·kg-1·h-1), or saline vehicle, and 6 h later the rats were subjected to 30 min of renal ischemia or to sham operation. Renal function was assessed by measurement of plasma creatinine at 24 and 48 h after renal I/R injury in the presence or absence of chronic infusions of local anesthetics and correlated to histological changes indicative of necrosis. The degree of renal apoptosis was assessed by three methods: 1) DNA fragmentation detected by terminal deoxynucleotidyl transferase biotin-dUTP nick-end labeling staining, 2) DNA laddering detected after agarose gel electrophoresis, and 3) morphological identification of apoptotic tubules at the corticomedullary junction. We also measured the expression of the proinflammatory markers ICAM-1 and TNF-α. Continuous local anesthetic infusion with renal I/R injury resulted in an increased magnitude and duration of renal dysfunction compared with the saline-infused I/R group. Additionally, both apoptotic and necrotic renal cell death as well as inflammatory changes were significantly potentiated in local anesthetic-treated rat kidneys. Local anesthetic infusion alone without I/R injury had no effect on renal function. We conclude that local anesthetics potentiated renal injury after I/R by increasing necrosis, apoptosis, and inflammation.

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Ischemic preconditioning and morphine attenuate myocardial apoptosis and infarction after ischemia-reperfusion in rabbits: role of δ-opioid receptor

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01143.2003 ◽

2004 ◽

Vol 287 (4) ◽

pp. H1786-H1791 ◽

Cited By ~ 42

Author(s):

Shinji Okubo ◽

Yujirou Tanabe ◽

Kenji Takeda ◽

Michihiko Kitayama ◽

Seiyu Kanemitsu ◽

...

Keyword(s):

Infarct Size ◽

Opioid Receptor ◽

Ischemic Preconditioning ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Terminal Deoxynucleotidyl Transferase ◽

Control Group ◽

Apoptotic Cells ◽

Protective Effects ◽

Δ Opioid Receptor

We examined whether ischemic preconditioning (IPC) attenuates ischemia-reperfusion injury, in part, by decreasing apoptosis and whether the δ-opioid receptor (DOR) plays a pivotal role in the regulation of apoptosis. Rabbits were subjected to 30-min coronary artery occlusion (CAO) and 180 min of reperfusion. IPC was elicited with four cycles of 5-min ischemia and 10-min reperfusion before CAO. Morphine (0.3 mg/kg iv) was given 15 min before CAO. Naloxone (Nal; 10 mg/kg iv) and naltrindole (Nti; 10 mg/kg iv), the respective nonselective and selective DOR antagonists were given 10 min before either morphine or IPC. Infarct size (%risk area) was reduced from 46 ± 3.8 in control to 11.6 ± 1.0 in IPC and 19.5 ± 3.8 in the morphine group (means ± SE; P < 0.001 vs. control). Nal blocked the protective effects of IPC and morphine, as shown by the increase in infarct size to 38.6 ± 7.2 and 44.5 ± 1.8, respectively. Similarly, Nti blocked IPC and morphine-induced protection. The percentage of apoptotic cells (revealed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) decreased in IPC (3.6 ± 1.9) and morphine groups (5.2 ± 1.2) compared with control group (12.4 ± 1.6; P < 0.001). Nti pretreatment increased apoptotic cells 11.2 ± 2.2% in IPC and 12.1 ± 0.8% in morphine groups. Nal failed to block inhibition of apoptosis in the IPC group (% of cells: 5.7 ± 1.3 vs. 3.6 ± 1.9 in IPC alone; P > 0.05). These results were also confirmed by nucleosomal DNA laddering pattern. We conclude that IPC reduces lethal injury, in part, by decreasing apoptosis after ischemia-reperfusion and activation of the DOR may play a crucial role in IPC or morphine-induced myocardial protection.

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ADAM8 Activates NLRP3 Inflammasome to Promote Cerebral Ischemia-Reperfusion Injury

Journal of Healthcare Engineering ◽

10.1155/2021/3097432 ◽

2021 ◽

Vol 2021 ◽

pp. 1-14

Author(s):

Hongwei Lu ◽

Yaqin Meng ◽

Xinrui Han ◽

Wei Zhang

Keyword(s):

Cerebral Ischemia ◽

Inflammatory Response ◽

Nlrp3 Inflammasome ◽

Transmembrane Protein ◽

Ischemia Reperfusion ◽

Cortical Cell ◽

Ischemic Injury ◽

Neurological Deficits ◽

Cerebral Ischemic Injury ◽

Cerebral Ischemic

Stroke is the leading cause of death and disability in humans. Strokes are classified as either ischemic or hemorrhagic. Ischemic stroke accounts for 70–80% of the cases. Inflammation is a key factor in ischemic brain injury. Studies have shown that inflammatory response induced by NLRP3 inflammasome is one of the root causes of brain damage in mice with cerebral ischemia. However, its specific mechanism in cerebral ischemia is still unclear. ADAM8 (a disintegrin and metalloproteases 8) is a transmembrane protein with different functions. It plays an important role in tumors and neuroinflammation-related diseases. However, the role and molecular mechanism of ADAM8 in cerebral ischemia injury are still unclear. This study aims to evaluate the role of ADAM8 in cerebral ischemic injury and explore its signal transduction mechanism. This experiment shows that ADAM8 can significantly cause neurological deficits in MCAO mice and can substantially cause ipsilateral cerebral edema and cerebral infarction in MCAO mice. In addition, ADAM8 can significantly induce cortical cell apoptosis in MCAO mice, leading to the loss of neurons and the expression of proinflammatory factors COX2, iNOS, TNFα, and IL-6. Importantly, we confirmed that ADAM8 mediates the inflammatory response by promoting the activation of NLRP3 inflammasome, microglia, and astrocytes. These results indicate that ADAM8 may be a candidate drug target for the prevention and treatment of the cerebral ischemic injury.

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Neuroprotective Effects of Ginsenosides against Cerebral Ischemia

Molecules ◽

10.3390/molecules24061102 ◽

2019 ◽

Vol 24 (6) ◽

pp. 1102 ◽

Cited By ~ 15

Author(s):

Zhekang Cheng ◽

Meng Zhang ◽

Chengli Ling ◽

Ying Zhu ◽

Hongwei Ren ◽

...

Keyword(s):

Cerebral Ischemia ◽

Ischemia Reperfusion ◽

Ischemic Injury ◽

Neurological Dysfunction ◽

Control Group ◽

Protective Effects ◽

Ginsenoside Rb1 ◽

Neuroprotective Effects

Ginseng has been used worldwide as traditional medicine for thousands of years, and ginsenosides have been proved to be the main active components for their various pharmacological activities. Based on their structures, ginsenosides can be divided into ginseng diol-type A and ginseng triol-type B with different pharmacological effects. In this study, six ginsenosides, namely ginsenoside Rb1, Rh2, Rg3, Rg5 as diol-type ginseng saponins, and Rg1 and Re as triol-type ginseng saponins, which were reported to be effective for ischemia-reperfusion (I/R) treatment, were chosen to compare their protective effects on cerebral I/R injury, and their mechanisms were studied by in vitro and in vivo experiments. It was found that all ginsenosides could reduce reactive oxygen species (ROS), inhibit apoptosis and increase mitochondrial membrane potential in cobalt chloride-induced (CoCl2-induced) PC12 cells injury model, and they could reduce cerebral infarction volume, brain neurological dysfunction of I/R rats in vivo. The results of immunohistochemistry and western blot showed that the expression of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), silencing information regulator (SIRT1) and nuclear transcription factor P65 (NF-κB) in hippocampal CA1 region of some ginsenoside groups were also reduced. In general, the effect on cerebral ischemia of Rb1 and Rg3 was significantly improved compared with the control group, and was the strongest among all the ginsenosides. The effect on SIRT1 activation of ginsenoside Rb1 and the inhibition effect of TLR4/MyD88 protein expression of ginsenoside Rb1 and Rg3 were significantly stronger than that of other groups. The results indicated that ginsenoside Rg1, Rb1, Rh2, Rg3, Rg5 and Re were effective in protecting the brain against ischemic injury, and ginsenoside Rb1 and Rg3 have the strongest therapeutic activities in all the tested ginsenosides. Their neuroprotective mechanism is associated with TLR4/MyD88 and SIRT1 activation signaling pathways, and they can reduce cerebral ischemic injury by inhibiting NF-κB transcriptional activity and the expression of proinflammatory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6).

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Effect of heat shock preconditioning on NF-κB/I-κB pathway during I/R injury of the rat liver

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00466.2001 ◽

2002 ◽

Vol 282 (6) ◽

pp. G962-G971 ◽

Cited By ~ 38

Author(s):

Hiroshi Uchinami ◽

Yuzo Yamamoto ◽

Makoto Kume ◽

Kei Yonezawa ◽

Yasuhide Ishikawa ◽

...

Keyword(s):

Heat Shock ◽

Messenger Rna ◽

Ischemia Reperfusion ◽

Nuclear Factor Κb ◽

Control Group ◽

Nuclear Factor ◽

Fatal Complication ◽

Hepatic Ischemia ◽

Proinflammatory Mediators ◽

Hepatic Ischemia Reperfusion

Hepatic ischemia-reperfusion (I/R) injury continues to be a fatal complication after liver surgery. Heat shock (HS) preconditioning is an effective strategy for protecting the liver from I/R injury, but its exact mechanism is still unclear. Because the activation of nuclear factor-κB (NF-κB) is an important event in the hepatic I/R-induced inflammatory response, the effect of HS preconditioning on the pathway for NF-κB activation was investigated. In the control group, NF-κB was activated 60 min after reperfusion, but this activation was suppressed in the HS group. Messenger RNA expressions of proinflammatory mediators during reperfusion were also reduced with HS preconditioning. Concomitant with NF-κB activation, NF-κB inhibitor I-κB proteins were degraded in the control group, but this degradation was suppressed in the HS group. This study shows that HS preconditioning protected the liver from I/R injury by suppressing the activation of NF-κB and the subsequent expression of proinflammatory mediators through the stabilization of I-κB proteins.

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Monocytes Undergo Functional Reprogramming to Generate Immunosuppression through HIF-1α Signaling Pathway in the Late Phase of Sepsis

Mediators of Inflammation ◽

10.1155/2020/4235909 ◽

2020 ◽

Vol 2020 ◽

pp. 1-9 ◽

Cited By ~ 1

Author(s):

Li-Li Li ◽

Bing Dai ◽

Yu-Han Sun ◽

Ting-Ting Zhang

Keyword(s):

Clinical Study ◽

Inflammatory Response ◽

Signaling Pathway ◽

Animal Study ◽

Inflammatory Responses ◽

Late Phase ◽

Severe Pneumonia ◽

Control Group ◽

L1 Protein ◽

Control Injection

Severe pneumonia with sepsis is characterized by a dysregulated inflammatory response of endotoxin. In our study, we attempted to investigate the roles of the immune guardian cells (monocytes) in the immune-inflammatory response of severe pneumonia-induced sepsis. We performed analysis in the blood samples of human and animals with ELISA, western blot, flow cytometry (FCM) methods, etc. Results showed that the proinflammatory status shifted to hypoinflammatory phases during the sepsis process. In a clinical study, the levels of IL-1β, IL-6, TNF-α, etc., except for IL-10, were inhibited in the late phase of sepsis, while, in an animal study, the immune suppression status was attenuated with administration of the adenovirus Ade-HIF-1α. Conversely, the amount of IL-10 was lower in the adenovirus Ade-HIF-1α group compared with the sepsis model group and the Ade-control group. Moreover, in the clinical study, the programmed cell death-ligand 1 (PD-L1) was overexpressed in monocytes in the late phase of sepsis, while the expression of proteins HIF-1α and STAT3 was decreased in the late phase of sepsis. However, in the animal study, we found that the HIF-1α factor facilitated the inflammatory response. The expression of the proteins HIF-1α and STAT3 was increased, and the PD-L1 protein was decreased with the adenovirus Ade-HIF-1α administration compared with the rats without Ade-HIF-1α injection and with the Ade-control injection. Additionally, the proteins HIF-1α and STAT3 were coregulated at transcriptional levels during the inflammatory responses of sepsis. Taken together, monocytes undergo reprogramming to generate immunosuppression through the HIF-1α signaling pathway in the late phase of sepsis.

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Establishment of a systemic inflammatory response syndrome model and evaluation of the efficacy of umbilical cord mesenchymal stem cell transplantation

10.21203/rs.3.rs-32086/v1 ◽

2020 ◽

Author(s):

Guangping Ruan ◽

Xiang Yao ◽

Mi-yang Liu-Gao ◽

Jin-xiang Wang ◽

Xue-min Cai ◽

...

Keyword(s):

Renal Function ◽

Treatment Group ◽

Systemic Inflammatory Response Syndrome ◽

Liver Function ◽

Inflammatory Response ◽

Umbilical Cord ◽

Heart Function ◽

Control Group ◽

Model Group ◽

Tree Shrews

Abstract Based on the characteristics of modern weapon injury, a repetitive model of traumatic systemic inflammatory response syndrome (SIRS) and an evaluation system were established. The models were treated with GFP-labeled tree shrew umbilical cord mesenchymal stem cells (UCMSCs). Forty out of 50 tree shrews were used to make a unilateral femoral comminuted fracture. LPS was injected intravenously to create a traumatic SIRS model. The other 10 shrews were used as normal controls. After the model was established for 10 days, 20 tree shrews were injected in the veins with GFP-labeled UCMSCs, and 18 tree shrews were not injected as the model control group. The distribution of GFP-labeled cells in vivo was measured at 2 and 10 days after injection. Twenty days after treatment, the model group, the normal control group, and the treatment group were taken to observe the pathological changes in each tissue, and blood samples were taken for the changes in liver function, renal function and heart function. Distribution of GFP-positive cells was observed in all tissues at 2 and 10 days after injection. After treatment, the HE staining results of the treatment group were close to those of the normal group, and the model group had a certain degree of lesions. The results of liver function, renal function and heart function tests in the treatment group were returned to normal, and the results in the model group were abnormally increased. UCMSCs have a certain effect on the treatment of traumatic SIRS and provide a new technical solution for modern weapon trauma treatment.

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