S-Nitrosoglutathione protects acute kidney injury in septic rats by inhibiting the activation of NLRP3 inflammasome.

Objectives: We aimed to study the effect of S-nitroso glutathione (SNG) on acute kidney injury (AKI) in septic rats by regulating nucleotide oligomerization domain-like receptor protein 3 (NLRP3). Materials and Methods: Sprague Dawley rats were used to construct the AKI model, and biochemical methods were used to detect the levels of inflammatory factors and anti-oxidant enzymes in renal tissue. We observed the ultrastructural changes of renal tissue by transmission electron microscopy and detected the protein and mRNA levels of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain foci (ASC) and caspase-1 by western-blotting and RT-qPCR. Results: Cecal ligation and puncture induced renal tubular epithelial tissue damage in septic rats, resulting in decreased renal function, increased levels of inflammation and decreased levels of anti-oxidant enzymes in renal tissue, and aggravated mitochondrial damage, significantly decreased mitochondrial density and enzyme complex I/II/III/IV levels (all P<0.001), and increased the protein and mRNA expression of NLRP3, ASC, and caspase-1 (all P<0.001). However, after pretreatment with SNG, the pathological damage of renal tubular epithelial tissue was reduced, the renal function was improved, the level of inflammation in renal tissue decreased and the level of anti-oxidant enzymes increased, the density of mitochondria and the level of enzyme complex I/II/III/IV were significantly increased (all P<0.001), meanwhile the protein and mRNA levels of NLRP3, ASC, and caspase-1 were all decreased significantly (all P<0.05). Conclusion: SNG protects AKI in septic rats by inhibiting NLRP3 inflammasome activation.

Protective effect of N-acetylcysteine on acute lung injury in septic rats by inhibiting inflammation, oxidation, and apoptosis.

Objectives: Acute lung injury (ALI) is a common comorbidity in patients with sepsis, and finding drugs that can effectively reduce its mortality is a hot spot in current research. The purpose of this study is to explore the protective mechanism of N-acetylcysteine (NAC) on ALI in septic rats. Materials and Methods: We used NAC to intervene in septic rats to evaluate the plasma inflammatory factors and lung tissue pathological damage. Biochemical methods were used to determine the levels of oxidases in lung tissue, the expression of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) proteins, and observed lung tissue cell apoptosis. Results: NAC pretreatment decreased the mortality of septic rats, improved lung tissue pathological damage, reduced the levels of tumor necrosis factor-α, interleukin-1ß, interleukin-6, interleukin-8, and malondialdehyde, and increased activity of superoxide dismutase, glutathione peroxidase, and catalase. Moreover, NAC pretreatment significantly decreased iNOS protein expression and increased eNOS protein expression in lung tissue. Meanwhile, NAC significantly decreased the number of apoptosis and the levels of Bax and Caspase-3 mRNA and increased the level of Bcl-2 mRNA in the lung tissue of septic rats. Conclusion: NAC protects ALI in septic rats by inhibiting inflammation, oxidative stress, and apoptosis.

Salidroside Protects Acute Kidney Injury in Septic Rats by Inhibiting Inflammation and Apoptosis.

Purpose: To clarify the protective effect and mechanism of salidroside (SLDS) on acute kidney injury (AKI) in septic rats. Methods: We pretreated rats with different doses of SLDS and analyzed the impact of SLDS on the survival of septic rats. We evaluated the levels of inflammatory factors in rats, the expression of NF-ƙB p65 in the kidney, and the apoptosis of kidney tubular epithelial cells (KTECs). Results: SLDS significantly decreased the mortality of septic rats, and it reduced the levels of TNF-α, IL-1ß, and IL-17A in plasma and kidneys and decreased the levels of serum creatinine, plasma renal injury molecule-1 and plasma neutrophil gelatin-associated lipocalin. Moreover, SLDS could significantly decrease the expression of NF-ƙB p65 in kidney tissues and the apoptotic number of KETCs, while reducing the mRNA levels of Caspase-3 and Bax mRNA, and increasing the level of Bcl-2 mRNA. Conclusion: SLDS pretreatment protects against AKI in septic rats by inhibiting the inflammation of kidney and the apoptosis of KTECs.

Sirtuin 3 deficiency promotes acute kidney injury induced by sepsis via mitochondrial dysfunction and apoptosis.

OBJECTIVES: To explore the regulation mechanism of Sirtuin 3 (SIRT3) on the mitochondrial function and apoptosis of acute kidney injury (AKI) in septic mice. MATERIALS AND METHODS: The sepsis-induced AKI model was constructed in the wild-type and SIRT3 knockout (KO) mice, and the levels of serum creatinine (Scr) and plasma kidney injury molecule 1 (pKIM-1) in mice were detected by ELISA. The mitochondrial damage of kidney tubular epithelial cells (KTEC) was observed by electron microscopy, the apoptosis of KTEC was detected by TUNEL assay, and the mRNA levels of SIRT3, Bax, Caspase-3, and Bcl-2 were detected by RT-qPCR. RESULTS: SIRT3 KO caused increased expression of Scr, pKIM-1, and inducible nitric oxide synthase protein in the kidneys of septic mice, and decreased the levels of superoxide dismutase, catalase, and mitochondrial complex enzymes I/II/III/IV. SIRT3 deficiency exacerbated histopathological and mitochondrial damage to the proximal tubules of the kidney. In addition, SIRT3 KO resulted in a significantly increased apoptosis of KTEC, increased the mRNA levels of Bax and Caspase-3, and decreased the mRNA levels of Bcl-2. CONCLUSION: Our study suggests that SIRT3 deficiency promotes sepsis-induced AKI via increasing oxidative stress, mitochondrial dysfunction, and inducing apoptosis.

Pretreatment with S-Nitrosoglutathione Attenuates Septic Acute Kidney Injury in Rats by Inhibiting Inflammation, Oxidation, and Apoptosis.

OBJECTIVE: We aimed to investigate the protective effect of s-nitrosoglutathione (SNG) pretreatment on acute kidney injury (AKI) in septic rats. METHODS: We constructed a rat model of sepsis by cecal ligation and puncture and observed the survival of the rats. We obtained kidney and blood samples from rats, observed the pathological damage to the kidney tissues, and evaluated kidney function and the expression levels of inflammatory factors. We also detected the expression of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the kidneys by immunohistochemistry and evaluated the apoptosis of kidney tubular epithelial cells (KTEC) by TUNEL. RESULTS: Pretreatment with SNG significantly reduced the mortality of septic rats, attenuated kidney pathological damage, and decreased the levels of serum creatinine, plasma neutrophil gelatinase-associated lipocalin, and plasma kidney injury molecule-1. Moreover, SNG pretreatment decreased the levels of TNF-α and IL-1ß in serum and kidney and reduced the expressions of NO, iNOS, PGE2, and COX-2 in the kidneys. Furthermore, pretreatment with SNG significantly reduced the apoptotic rate of KTEC and decreased the levels of caspase-3 and Bax mRNA, but increased the level of Bcl-2 mRNA. CONCLUSION: Pretreatment with SNG has a protective effect on AKI in septic rats, and the specific mechanisms are related to inhibition of inflammation, oxidation, and apoptosis.

Protective Effect of N-Acetylcysteine Pretreatment on Acute Kidney Injury in Septic Rats.

BACKGROUND: The aim of this study is to investigate the protective effect of N-acetylcysteine (NAC) pretreatment on acute kidney injury in septic rats. METHODS: We constructed a septic rat model by cecal ligation and perforation (CLP) and assessed kidney tissue pathologic damage, renal function changes, and inflammatory factor levels. Meanwhile, we also assessed oxide and antioxidant enzyme levels in kidney tissues, observed apoptosis of kidney tissues, and evaluated mitochondrial membrane activity in renal cortical cells. RESULTS: Pretreatment of NAC significantly alleviated pathologic damage of kidney tissues in septic rats; decreased the levels of serum creatinine, blood urea nitrogen, plasma neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1; and reduced the expression of tumor necrosis factor a, interleukin [IL]-1ß, IL-6, and IL-8. Furthermore, NAC pretreatment reduced the level of protein-nitrotyrosine adducts and malondialdehyde in CLP-induced kidney tissues, while elevated the levels of superoxide dismutase, glutathione peroxidase, and catalase. Moreover, pretreatment of NAC reduced the number of apoptosis in kidney tissues induced by CLP, decreased the mRNA levels of caspase-3, caspase-9, cytochrome c, and poly ADP-ribose polymerase, and increased mitochondrial membrane activity in renal cortical cells (complex I/II/III/IV). CONCLUSIONS: NAC pretreatment has protective effects on acute kidney injury induced by CLP, and its mechanism is closely related to anti-inflammatory, antioxidation, antiapoptosis, and regulation of mitochondrial function.

Thrombocytopenia as a predictor of severe acute kidney injury in patients with heat stroke.

BACKGROUND: Abnormalities of blood system often occur several days before acute kidney injury (AKI) in patients with heat stroke (HS). We aimed to investigate the prevalence and prognostic value of the early hematological markers in patients with AKI induced by HS. METHODS: In a retrospective cohort study, we analyzed the case records of 176 patients with HS and evaluated the hematological markers for early prediction and risk classification in the patients with AKI. RESULTS: Of 176, 103 (58%) HS cases developed AKI, and men comprised more than half (75%) of the sample population. The nadir platelet count significantly correlated with the levels of peak serum creatinine (r = -0.608, p < 0.01) and blood urea nitrogen (r = -0.546, p < 0.01), and the length of hospital stay (r = -0.393, p < 0.01). The areas under the receiver operating characteristic curves (AU-ROC) indicated the prognostic accuracy of hematological markers, AU-ROC was significantly higher with the nadir platelet count than that with the admission platelet count (AU-ROC of the nadir platelet: 0.73; 95% CI: 0.67-0.82; vs. AU-ROC of the admission platelet: 0.67; 95% CI: 0.59-0.75; p < 0.01). Multiple logistic regression results indicated that the nadir platelet count (adjusted ORs: 37.92; 95% CI: 2.18-87.21; p < 0.01) was independent predictor of AKI in HS. CONCLUSION: The high mortality observed in HS complicated with AKI, and among the various hematological parameters assessed, thrombocytopenia is associated with AKI induced by HS independently.

[The study of EEG Higher Order Spectral Analysis technology].

The basic theory of Higher Order Spectral Analysis and the most generally used Bispectrum are introduced in the paper. By certain experiments of EEG signal acquisition and bispectrum analysis, it is showed that the Higher Order Spectrum has an advantage over power spectrum, which is based on Second Order Statistics, in processing non-linear signal and restraining Gauss noise signal.

[Methods of extracting AEP for monitoring the anesthetic depth].

Many researches have proved that auditory evoked potentials (AEP) can indicate the depth of anesthesia in the clinical practice. This paper introduces two methods of extracting AEP: the moving time average (MTA) model and the autoregressive model with exogenous input (ARX). In our study we used both the MTA model and the ARX model to extract AEP and the results show that using the ARX model can get the results significantly faster than using the MTA model, and the ARX model is more suitable for the real-time monitoring of the anesthetic depth.

[Study on digital radiography equilibrium processing].

On account of different thickness of tissues absorbing different doses of X ray, it is difficult to display anatomical details of different tissues on a single screen of DR equipment. In order to resolve this problem, the self-adaptive reverse S mode transformation algorithm is presented in the paper, which can modify darker regions and brighter regions respectively, and improve the visibility of weakly details.

[A monitoring technique in detecting the depth of anesthesia by bispectral index].

At the present time, a kind of monitoring technology assuring highly effectual anesthesia is urgently required in the clinical practice. Electroencephalogram (EEG) assumes a dominant position in the current research of the depth detection of anesthesia. In this paper, the monitoring technique of the depth detection of anesthesia by bispectral index (BIS) is systematically showed. The bispectral index is a compound parameter which is composed of time domain, frequency domain, and high order spectral subparameters of the electroencephalograph. This nonlinear compound calculation method is worth research and is of great significance to the development of a new monitor of closed-loop control of anesthesia.