Analysis of Blood Trace Elements and Biochemical Indexes Levels in Severe Craniocerebral Trauma Adults with Glasgow Coma Scale and Injury Severity Score

Xu, Guangtao; Hu, Bo; Chen, Guiqian; Yu, Xiaojun; Luo, Juan; Lv, Jidong; Gu, Jiang

doi:10.1007/s12011-014-0225-z

Cited by 19 publications

(11 citation statements)

References 35 publications

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“…After cooling, the mixtures were made up to 10 mL with ultrapure water and stored in closed propylene tubes at 4 °C for use. Ca quantifications were performed by inductively coupled plasma atomic emission spectrophotometry (ICP-AES) (Bohui Innovation Technology, Beijing, China) as described previously [31-33]. Briefly, the aliquots of the mixtures were mineralized with nitric/sulfuric/perchloric acid (3: 1:1, v/v ) in closed Teflon vessels in order to eliminate interference from the organic matrixes.…”

Section: Methodsmentioning

confidence: 99%

Role of Calcium Sensing Receptor in Streptozotocin-Induced Diabetic Rats Exposed to Renal Ischemia Reperfusion Injury

Hu¹,

Tong²,

Xu³

et al. 2018

Kidney Blood Press Res

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Background/Aims: Renal ischemia/reperfusion (I/R) injury (RI/RI) is a common complication of diabetes, and it may be involved in altering intracellular calcium concentrations at its onset, which can result in inflammation, abnormal lipid metabolism, the production of reactive oxygen species (ROS), and nitroso-redox imbalance. The calcium-sensing receptor (CaSR) is a G-protein coupled receptor, however, the functional involvement of CaSR in diabetic RI/ RI remains unclear. The present study was intended to investigate the role of CaSR on RI/RI in diabetes mellitus (DM). Methods: The bilateral renal arteries and veins of streptozotocin (STZ)-induced diabetic rats were subjected to 45-min ischemia followed by 2-h reperfusion with or without R-568 (agonist of CaSR) and NPS-2143 (antagonist of CaSR) at the beginning of I/R procedure. DM without renal I/R rats served as control group. The expressions of CaSR, calmodulin (CaM), and p47phox in the renal tissue were analyzed by qRT-PCR and Western blot. The renal pathomorphology, renal function, oxidative stress, inflammatory response, and calcium disorder were evaluated by detection of a series of indices by hematoxylin-eosin (HE) staining, transmission electron microscope (TEM), commercial kits, enzyme-linked immunosorbent assay (ELISA), and spectrophotofluorometry, respectively. Results: Results showed that the expressions of CaSR, CaM, and p47phox in I/R group were significantly up-regulated as compared with those in DM group, which were accompanied by renal tissue injury, increased calcium, oxidative stress, inflammation, and nitroso-redox imbalance. Conclusion: These results suggest that activation of CaSR is involved in the induction of damage of renal tubular epithelial cell during diabetic RI/RI, resulting in lipid peroxidation, inflammatory response, nitroso-redox imbalance, and apoptosis.

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Section: Methodsmentioning

confidence: 99%

Role of Calcium Sensing Receptor in Streptozotocin-Induced Diabetic Rats Exposed to Renal Ischemia Reperfusion Injury

Hu¹,

Tong²,

Xu³

et al. 2018

Kidney Blood Press Res

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“…The renal function was evaluated through measurement of blood urea nitrogen (BUN) and serum creatinine (Scr) levels using Hitachi automatic biochemical analyzer 7060 c (Japan) and Roche Diagnostics kits (Mannheim, Germany) by the picric acid method according to the manufacturer’s instructions [22]. …”

Section: Methodsmentioning

confidence: 99%

Activation of Nrf2/HO-1 Pathway by Glycogen Synthase Kinase-3β Inhibition Attenuates Renal Ischemia/Reperfusion Injury in Diabetic Rats

Shen

et al. 2017

Kidney Blood Press Res

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Background/Aims: Diabetes mellitus can exacerbate renal ischemia-reperfusion (I/R) injury (RI/RI). The aim of the present study was to evaluate the protective effect of GSK-3β inhibition (TDZD-8) on I/R-induced renal injury through the Nrf2/HO-1 pathway in a streptozocin (STZ)-induced diabetic rat model. Methods: STZ-induced diabetic rats preconditioned with TDZD-8 and ZnPP were subjected to renal I/R. The extent of renal morphologic lesions. Renal function was assessed from blood urea nitrogen (BUN) and serum creatinine (Scr), as determined utlizing commercial kits. Oxidative stress and inflammatory activity in the kidney tissue was estimated from levels of malondialdehyde (MDA), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), as well as the activities of superoxide dismutase (SOD) and glutathione (GSH) using qRT-PCR and ELISA. The expressions of Nrf2, HO-1, Bcl-2 and NF-κB in the renal tissue were measured by qRT-PCR and western blotting. Results: I/R-induced renal inflammation was reduced significantly by TDZD-8 pretreatment. Preconditioning with TDZD-8 suppressed NF-κB expression and enhanced Bcl-2 expression in the renal tissue. The upregulated level of malondialdehyde (MDA), and reduced activities of superoxide dismutase (SOD) and glutathione (GSH) in I/R-shocked rats were markedly restored by TDZD-8 pretreatment. Furthermore, pretreatment with TDZD-8 enhanced activation of the Nrf2/HO-1 pathway in the renal tissue of diabetic RI/RI rats. Conclusion: These findings suggest that preconditioning with TDZD-8 may protect the kidney from I/R-induced damage via the activation of the Nrf2/HO-1 pathway in STZ-induced diabetic rats. Further detailed studies are needed to further clarify the underlying mechanisms.

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“…Previous studies confirm that severe trauma induces acute trace element deficiency and its redistribution of the imbalance, which may be an underlying mechanism for biochemical metabolism, pathophysiology, and pathological anatomy of secondary SIRS, MODS/MOF, and death. [ 7 – 14 ] The absolute and relative concentrations of TEs in both critical care and conventional treatment, which can lead to acute trace element deficiency (ATED), constitute an important mechanism of MODS/MOF, SIRS, and death. [ 15 , 16 ] In this study, we investigate the early acute changes of blood zinc, iron, and copper in patients with multiple fractures, with the intent to verify the theory of acute trace elements from the clinical point of view.…”

Section: Introductionmentioning

confidence: 99%

Changes of serum trace elements in early stage trauma and its correlation with injury severity score

Chen

Lv²,

Wang³

et al. 2018

Medicine

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BackgroundSevere trauma can cause secondary multiple organ dysfunction syndrome and death. The absolute and relative concentrations of trace elements in both critical care and conventional treatment, which can lead to acute trace element deficiency, constitute an important mechanism of multiple organ dysfunction syndrome (MODS)/multiple organ failure (MOF).MethodsWe investigated the changes in serum Cu, Zn, and Fe in early stage trauma of patients with the high injury severity score (ISS) and correlated the change in trace elements with ISS. Blood samples were collected within an hour of admittance and the patients were scored according to ISS. We collected clinical data records and ISS score values, and determined serum Fe, Zn, and Cu by inductively coupled plasma mass spectrometry.ResultsCompared with the control group, the serum Zn and Fe values of trauma patients were decreased. There was no significant difference in serum Cu between the patients and the control group. In the trauma group, the serum Zn and Fe were lower than that of the minor injury group, and the difference of Cu concentration was not statistically significant.ConclusionsSerum Zn and Fe levels in patients with multiple trauma fractures were significantly different than those in the normal group, suggesting that Zn and Fe need to be monitored in the early stage of trauma.

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Analysis of Blood Trace Elements and Biochemical Indexes Levels in Severe Craniocerebral Trauma Adults with Glasgow Coma Scale and Injury Severity Score

Cited by 19 publications

References 35 publications

Role of Calcium Sensing Receptor in Streptozotocin-Induced Diabetic Rats Exposed to Renal Ischemia Reperfusion Injury

Role of Calcium Sensing Receptor in Streptozotocin-Induced Diabetic Rats Exposed to Renal Ischemia Reperfusion Injury

Activation of Nrf2/HO-1 Pathway by Glycogen Synthase Kinase-3β Inhibition Attenuates Renal Ischemia/Reperfusion Injury in Diabetic Rats

Changes of serum trace elements in early stage trauma and its correlation with injury severity score

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