Effect of "micromovement" in preventing intraoperative acquired pressure injuries among patients undergoing surgery in supine position.

To explore the clinical effect of "micromovement" in preventing intraoperative acquired pressure injures (IAPIs) among patients experiencing surgery in supine position. A total of 200 patients accepting elective surgery in supine position from 10 May 2023 to 4 July 2023 at Shulan (Hangzhou) Hospital were selected and randomized into two groups (experimental group, n = 100; control group, n = 100). For control group patients, soft silicone foam dressing was applied to the sacrococcygeal region. On the basis of the treatment for control group patients, "micromovement" was implemented among experimental group patients. During this process, the operating table was tilted for 15° leftwards and rightwards alternately every 1 h, and the tilt angle was maintained for 5 min to prevent IAPIs. Finally, comparisons between the two groups were made in terms of the sacrococcygeal IAPI incidence, relative temperature differences (ΔT) on sacrococcygeal skin, and job satisfaction of nurses. Compared with control group patients, patients from the experimental group exhibited lower IAPI incidence (2% vs. 10%), reduced ΔT between the sacrococcygeal skin and surrounding normal skin [0 (-0.1, 0.1) vs. 0.2 (-0.2, 0.4)], and elevated job satisfaction of nurses (80% vs. 66%). All the differences were statistically significant (p < 0.05). "Micromovement" implemented intraoperatively among patients receiving surgery in supine position is able to lower the IAPI incidence by five times and elevate job satisfaction of nurses.

Effect of Yulangsan Polysaccharide on the Reinstatement of Morphine-Induced Conditioned Place Preference in Sprague-Dawley Rats.

We previously reported that Yulangsan polysaccharide (YLSP), which was isolated from the root of Millettia pulchra Kurz, attenuates withdrawal symptoms of morphine dependence by regulating the nitric oxide pathway and modulating monoaminergic neurotransmitters. In this study, we investigated the effects and mechanism of YLSP on the reinstatement of morphine-induced conditioned place preference (CPP) in rats. A CPP procedure was employed to assess the behavior of rats, and indicators of serum and four brain regions (nucleus accumbens, ventral tegmental area, hippocampus and prefrontal cortex) were determined to explore its underlying mechanism. YLSP inhibited priming morphine-induced reinstatement of CPP in a dose-dependent manner. YLSP markedly reduced nitric oxide and nitric oxide synthase levels in the brain. Moreover, YLSP significantly decreased the dopamine and norepinephrine levels in the serum and brain. Furthermore, YLSP significantly decreased cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) concentrations, inhibited the expression of dopamine D1 receptors and cAMP response element binding protein mRNA, and improved the expression of dopamine D2 receptor mRNA in the four brain regions. Our findings indicated that YLSP could inhibit the reinstatement of morphine-induced CPP possibly by modulating the NO-cGMP and D1R-cAMP signaling pathways.

The Antioxidant, Anti-Inflammatory and Anti-Apoptotic Activities of the Bauhinia Championii Flavone are Connected with Protection Against Myocardial Ischemia/Reperfusion Injury.

BACKGROUND/AIMS: Previous studies have demonstrated that Bauhinia championii flavone (BCF) exhibits anti-oxidative, anti-hypoxic and anti-stress properties. This study was designed to investigate whether BCF has a cardioprotective effect against myocardial ischemia/reperfusion (I/R) injuries in rats and to shed light on its possible mechanism. METHODS: The model of I/R was established by ligating the left anterior descending coronary artery for 30 min, then reperfusing for 180 min. Hemodynamic changes were continuously monitored. The content of malondialdehyde (MDA) as well as the lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were assessed. The release of interleukin-6 (IL-6) was measured by enzyme-linked immunosorbent assay (ELISA). Apoptosis of cardiomyocytes was determined by caspase-3 activity and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The expression of TLR4, NF-x03BA;Bp65, Bcl-2 and Bax were detected by western blotting. RESULTS: Pretreatment with BCF significantly reduced the serum levels of LDH, MDA and IL-6, but increased the activities of SOD and GSH-Px. It also attenuated myocardial infarct size, reduced the apoptosis rate and preserved cardiac function. Furthermore, BCF inhibited caspase-3 activity and the expression of TLR4, phosphorylated NF-x03BA;Bp65 and Bax, but enhanced the expression of Bcl-2. CONCLUSION: These results provide substantial evidence that BCF exerts a protective effect on myocardial I/R injury, which may be attributed to attenuating lipid peroxidation, the inflammatory response and apoptosis.

Protective Effect of 2-Dodecyl-6-Methoxycyclohexa-2, 5-Diene-1, 4-Dione, Isolated from Averrhoa Carambola L., Against Palmitic Acid-Induced Inflammation and Apoptosis in Min6 Cells by Inhibiting the TLR4-MyD88-NF-κB Signaling Pathway.

BACKGROUND/AIMS: Studies have demonstrated that 2-dodecyl-6-methoxycyclohexa-2, 5-diene-1, 4-dione (DMDD), isolated from the roots of Averrhoa carambola L., has significant therapeutic potential for the treatment of diabetes. However, the protective effect of DMDD against pancreatic beta cell dysfunction has never been reported. We investigated whether DMDD protected against palmitic acid-induced dysfunction in pancreatic ß-cell line Min6 cells by attenuating the inflammatory response and apoptosis and to shed light on its possible mechanism. METHODS: Cell viability was assessed by CCK-8. Glucose-stimulated insulin secretion levels and inflammatory cytokines levels were examined by ELISA. Apoptosis was assessed by Annexin V-FITC/PI Flow cytometry assay, Hoechst 33342/PI double-staining assay, and Transmission electron microscopy assay. Relative quantitative real-time PCR and western blot were used to determine the expressions of genes and proteins. RESULTS: Cell viability and glucose-stimulated insulin secretion levels were increased in DMDD-pretreated Min6 cells. DMDD inhibited inflammatory cytokines IL-6, TNF-α and MCP-1 generations in palmitic acid (PA)-induced Min6 cells. Moreover, DMDD protected against PA-induced Min6 cells apoptosis and the expression of Cleaved-Caspase-3, -8 and -9 were down-regulated and the Bcl-2/Bax ratio was increased in DMDD-pretreated Min6 cells. In addition, the expression of TLR4, MyD88 and NF-κB were down-regulated in DMDD-pretreated Min6 cells and TAK-242-pretreated group cells. CONCLUSIONS: DMDD protected Min6 cells against PA-induced dysfunction by attenuating the inflammatory response and apoptosis, and its mechanism of this protection was associated with inhibiting the TLR4-MyD88-NF-κB signaling pathway.

The Effects of 17-Methoxyl-7-Hydroxy-Benzene-Furanchalcone on Pressure Overload-Induced Cardiac Remodeling in Rats and the Endothelial Mechanisms Based on PGI2.

AIM: The primary objective of this study was to study the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC) on pressure overload-induced cardiac remodeling in rats, as well as the endothelial mechanisms based on PGI2. METHODS: Six weeks following surgery, rats were divided randomly into the following groups: a sham group, a model group, an MHBFC 12 mg/kg/day group (MHBFC 12), an indomethacin 2 mg/kg/day group (Indo 2), and an Indo 2+ MHBFC 12 group. The MS 4000 organism signal system was used to record the rats' hemodynamic indices. Additionally, the heart weight was determined, and the cardiac remodeling index was calculated. HE and Masson's stains were utilized to perform histological analyses; the immunofluorescence was used to observe the microvessel density of myocardial tissue; the colorimetric method was used to determine the hydroxyproline content of cardiac tissue; the ELISA method was used to measure the plasma PGI2 content; and transmission electron microscopy was used to observe the ultrastructure of the myocardium. RESULTS: A hyperdynamic circulation state, cardiac remodeling, decreased microvessel density and decreased plasma PGI2 content were each observed in the model group compared with the sham group, in which any changes in the above parameters were effectively reversed by MHBFC. Single-use Indo administration resulted in the progression of these pathophysiological changes; however, MHBFC prevented the worsening of these parameters. CONCLUSION: MHBFC significantly reverses pressure overload-induced cardiac remodeling, and its mechanism may partially contribute to the amelioration of endothelial cell function and the augmentation of PGI2 synthesis and secretion.

Mechanism of the protective effect of Yulangsan flavonoid on myocardial ischemia/reperfusion injury in rats.

AIMS: Effect and mechanism of Yulangsan flavonoid (YLSF) on rat myocardial ischemia/reperfusion injury (MI/RI) has been investigated. METHODS: Sprague-Dawley (SD) rats were randomly divided into seven groups (sham group, model group and NS group: 2 mL of normal saline/kg body weight was administered; diltiazem group: 5 mg of diltiazem hydrochloride/kg body weight was administered; YLSFL, YLSFM and YLSFH groups: 20, 40 and 80 mg of YLSF/kg body weight was administered) and the MI/RI model was established. Myocardial infarct area, levels of myocardial enzymes and nitric oxide synthase (NOS) were measured. Caspase-3 and adenine nucleotide translocator-1 (ANT1) mRNA expression were evaluated by reverse transcription polymerase chain reaction (RT-PCR). Pathological structure and cardiocyte ultrastructure were also analysed. RESULTS: Compared with the MI/RI group, pretreatment with YLSF or diltiazem hydrochloride decreased the infarct area, levels of inducible nitric oxide synthase (iNOS), caspase-3 as well as the leakage of myocardial enzyme and increased activities of total nitric oxide synthase (tNOS) as well as constitutive nitric oxide synthase (cNOS). Cellular edema and the infiltration of inflammatory cells were alleviated. CONCLUSIONS: The experiment showed that YLSF protected the heart against MI/RI, possibly by reducing lipid peroxidation damage, regulating NOS activity and modulating the apoptosis genes expression.

Protective effects of total extracts of Averrhoa carambola L. (Oxalidaceae) roots on streptozotocin-induced diabetic mice.

BACKGROUND: In Chinese culture, the roots of Averrhoa carambola L. have long been used for medical purposes due to their potent pharmaceutical activities, such as improving digestive function and treating diabetes. METHODS: Recently, we prepared extracts of Averrhoa carambola L. root (EACR), which were isolated from Averrhoa carambola L. roots using ethanol or water. This study was designed to investigate the potential effects of EACR on streptozotocin (STZ) diabetic mice and to explore the underlying mechanism of these effects. Male mice were injected with STZ through the tail vein (120 mg/kg body weight) and were identified as a diabetic mouse model when the level of blood glucose was ≥11.1 mmol/L. Subsequently, the mice were administered EACR (150, 300, 600, 1200 mg/kg body weight/d) and metformin (320 mg/kg body weight/d) via intragastric gavage for three weeks. RESULTS: The results indicated that EACR significantly decreased the serum levels of blood glucose, total cholesterol (TC), triglycerides (TGs) and free fatty acids (FFAs), whereas the content of serum insulin was elevated. In addition, the expressions of apoptosis-related regulators (including caspase-3, caspase-8 and caspase-9) and the apoptosis-induced protein Bax were markedly down-regulated by EACR, whereas the expression of the anti-apoptotic Bcl-2 protein was notably increased. Furthermore, EACR could protect the diabetic mice against the STZ-induced apoptosis of pancreatic ß cells. CONCLUSION: Taken together, these findings indicate that EACR plays an effective hyperglycemic role that is associated with ameliorating metabolic functions and with inhibiting apoptosis in pancreas tissue.

MiR-7a-5p Attenuates Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis by Targeting VDAC1.

MicroRNA-7a-5p (miR-7a-5p) is closely related to apoptosis and plays an important role in ischemia/reperfusion (I/R) injury. Whether miR-7a-5p is involved in hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis is unknown. Therefore, this study aims to evaluate the role of miR-7a-5p in cardiomyocyte H9C2 cells in response to H/R stimulation. The results of RT-qPCR demonstrated that the expression level of miR-7a-5p was significantly down-regulated in H/R-treated H9C2 cells. MTT assay revealed that the cell viability was notably decreased in H/R group. Flow cytometric analysis found that the ratio of apoptotic cells was increased markedly following H/R. Enforced miR-7a-5p expression increased cell viability and decreased the apoptotic rate. Western blot analysis revealed that the expressions of pro-apoptotic proteins cleaved caspase-3 and Bax were down-regulated, while the expression of anti-apoptotic protein Bcl-2 was up-regulated in H/R-treated H9C2 cells transfected with miR-7a-5p mimic. On the contrary, miR-7a-5p downexpressing promoted apoptosis in H/R-treated H9C2 cells. Furthermore, the bioinformatics prediction manifested voltage-dependent anion channel 1 (VDAC1) was a potential target for miR-7a-5p, and dual-luciferase reporter assay confirmed that miR-7a-5p targeted VDAC1 3' untranslated regions, which leads to the repressed expressions of VDAC1 mRNA and protein. Knockdown of VDAC1 potentiated the protective effects of miR-7a-5p against H/R-induced cell injury. In conclusion, our results demonstrated that miR-7a-5p is involved in H/R-induced cardiomyocyte apoptosis through targeting VDAC1. MiR-7a-5p/VDAC1 axis might be utilized as hopeful biomarkers to reveal the potential mechanism of myocardial I/R injury.

Correction: The Effects of 17-Methoxyl-7-Hydroxy-Benzene-Furanchalcone on the Pressure Overload-Induced Progression of Cardiac Hypertrophy to Cardiac Failure.

[This corrects the article DOI: 10.1371/journal.pone.0091834.].

Efficacy and safety of transjugular intrahepatic portosystemic shunt combined with transcatheter embolization/chemoembolization in hepatocellular carcinoma with portal hypertension and arterioportal shunt.

OBJECTIVES: This study seeks to assess the efficacy and safety of transjugular intrahepatic portosystemic shunt (TIPS) combined with transarterial embolization/transarterial chemoembolization (TAE/TACE) in hepatocellular carcinoma (HCC) with portal hypertension and arterioportal shunt (APS). METHODS: Consecutive hospitalized patients having HCC accompanied by portal hypertension and APS were retrospectively analyzed. A total of 103 patients were enrolled. Of them, 26 patients were in Group A and 77 patients were in Group B according to the treatment protocol (Group A: TIPS plus TAE/TACE; Group B: TAE/TACE alone). The clinical outcomes and survival rate were compared between the two groups. RESULTS: The mean survival time in Group A and Group B were 14 mo and 9.9 mo, respectively, with statistical difference (p = 0.043). The immediate APS improvement rate was 95.2% in Group A and 91.9% in Group B, respectively, with no signficant difference (p = 1.000). However, the first follow-up consultation revealed that APS improvement rate in Group A was more obvious (66.7% vs 27.4%, p = 0.001). Objective response rate of HCC tended to be greater in Group A compared with Group B (65.4% vs 38.7%, p = 0.019). Liver function parameters significantly increased in Group A than those in Group B. After TIPS placement, the mean portal pressure gradient decreased from 32.61 ± 8.87 mmHg to 15.61 ± 8.15 mmHg, with significant difference (p = 0.000). The rate of absorption of ascites and control of variceal bleeding were statistically different between the two groups (p = 0.045 and 0.039, respectively). CONCLUSION: Our research suggests that TIPS combined with TAE/TACE seems to be safe and efficacious in patients with HCC accompanied by portal hypertension and APS, albeit may be accompanied by liver function damage.

Multidisciplinary treatment of advanced hepatocellular carcinoma with severe arterioportal shunt: a case report.

Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer mortality globally. In addition, most patients present in advanced stages with limited curative treatment options. Therefore, multidisciplinary treatment is often warranted. Here, we report a patient with HCC and severe arterioportal shunt (APS) who was treated with a multidisciplinary approach comprising interventional radiology procedures, apatinib and camrelizumab. After treatment, the intrahepatic mass was stable, and a notable decrease in the number and size of lung lesions was observed. The patient achieved a long-term survival of more than 2 years. These data suggest that multidisciplinary treatments may be effective in the treatment of advanced HCC with severe APS.

17-Methoxyl-7-Hydroxy-Benzene-Furanchalcone Ameliorates Myocardial Ischemia/Reperfusion Injury in Rat by Inhibiting Apoptosis and Autophagy Via the PI3K-Akt Signal Pathway.

17-Methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC), a monomer isolated from the root of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z. Wei (Papilionaceae), has been demonstrated to exhibit protective effects on myocardial ischemia/reperfusion (I/R) injury in rats. However, the mechanisms for the effect are not completely clear. In the present study, we tested whether MHBFC could reduce I/R-induced apoptosis and overautophagy via the PI3K-Akt pathway. The rat I/R model was established by ligating the left anterior descending coronary artery for 30 min and then followed by reperfusion for 2 h. MHBFC (10 mg/kg, intravenously) was administered alone or along with LY294002 (PI3K inhibitor, 0.3 mg/kg, intravenously) 5 min before the onset of reperfusion. We found that MHBFC postconditioning prevented I/R-induced release of creatine kinase-MB and tumor necrosis factor-α, inhibited the opening of mitochondrial permeability transition pore, and promoted nitric oxide production. Additionally, MHBFC caused a significant increase in PI3K, phosphorylation of Akt, mammalian target of rapamycin, and endothelial nitric oxide synthase, and a decrease in the expression of cleaved caspase-3, Beclin1, and conversion of microtubule-associated protein 1 light chain 3. However, the above functions of MHBFC were blocked by LY294002. These observations indicate that MHBFC plays a protective role against myocardial I/R injury by inhibiting apoptosis and excessive autophagy, which might be related to the activation of the PI3K-Akt signal pathway.

Epigallocatechin gallate exerts protective effects against myocardial ischemia/reperfusion injury through the PI3K/Akt pathway-mediated inhibition of apoptosis and the restoration of the autophagic flux.

Epigallocatechin gallate (EGCG), a polyphenol derived from green tea, exhibits a wide range of biological activities, including antioxidant, atherosclerosis and antitumor activities. In this study, the cardioprotective effects of EGCG on myocardial ischemia/reperfusion (I/R) injury in rats and the underlying mechanisms were investigated. A rat model of I/R injury was established by ligating the left anterior descending coronary artery for 30 min, followed by reperfusion for 2 h. The levels of I/R-induced creatine kinase-MB (CK-MB) and the release of lactate dehydrogenase (LDH), as well as the infarct size, cardiomyocyte apoptosis and cardiac functional impairment were examined and compared. Western blot analysis was carried out to elucidate the potential molecular mechanisms of action of EGCG. The results revealed that EGCG post-conditioning significantly decreased the levels of CK-MB and the release of LDH, reduced the myocardial infarct size, decreased the apoptotic rate and partially preserved heart function. Furthermore, EGCG decreased the expression of cleaved caspase-3 concomitantly with the upregulation of PI3K, and the phosphorylation of Akt and endothelial nitric oxide synthase (eNOS). It also inhibited I/R-induced overautophagy and promoted the clearance of autophagosomes, as evidenced by a decrease in the ratio of microtubule-associated protein 1 light chain 3 (LC3)-II/LC3-I, the downregulation of Beclin1, Atg5 and p62, and the upregulation of active cathepsin D. Additionally, we observed an increase in the phosphorylation levels of the mammalian target of rapamycin (mTOR) following treatment with EGCG. Taken together, the findings of this study demonstrate that, EGCG post-conditioning alleviates myocardial I/R injury by inhibiting apoptosis and restoring the autophagic flux, which is associated with several targets of the PI3K/Akt signaling pathway.

Bauhinia championii flavone inhibits apoptosis and autophagy via the PI3K/Akt pathway in myocardial ischemia/reperfusion injury in rats.

This study aimed to determine the effects of Bauhinia championii flavone (BCF) on myocardial ischemia/reperfusion injury (MI/RI) in rats and to explore potential mechanisms. The MI/RI model in rats was established by ligating the left anterior descending coronary artery for 30 minutes, then reperfusing for 3 hours. BCF at 20 mg/kg was given 20 minutes prior to ischemia via sublingual intravenous injection, with 24 µg/kg phosphoinositide 3-kinase inhibitor (PI3K; wortmannin) as a control. The creatine kinase-MB and nitric oxide content were assessed by colorimetry. The levels of mitochondrial permeability transition pores and tumor necrosis factor alpha were determined by an enzyme-linked immunosorbent assay. Cardiomyocyte apoptosis was detected by the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Additionally, the expression of PI3K, endothelial nitric oxide synthase, caspase-3, and Beclin1 was analyzed by fluorescence quantitative polymerase chain reaction and Western blotting, respectively. Akt and microtubule-associated protein 1 light chain 3-II protein levels were also evaluated. Pretreatment with BCF significantly decreased the levels of creatine kinase-MB, tumor necrosis factor alpha, and mitochondrial permeability transition pores, but increased the nitric oxide content. Furthermore, BCF inhibited apoptosis, downregulated caspase-3, Beclin1, and microtubule-associated protein 1 light chain 3-II, upregulated PI3K, and increased the protein levels of phosphorylated Akt and endothelial nitric oxide synthase. However, all of the previously mentioned effects of BCF were blocked when BCF was coadministered with wortmannin. In conclusion, these observations indicated that BCF has cardioprotective effects against MI/RI by reducing cell apoptosis and excessive autophagy, which might be related to the activation of the PI3K/Akt signaling pathway.

The effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone on the pressure overload-induced progression of cardiac hypertrophy to cardiac failure.

We investigated the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC), which was isolated from the roots of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z.Wei (Papilionaceae) (MKL), on the progression of cardiac hypertrophy to failure in a rat model of abdominal aortic banding (AAB)-induced pressure overloading. Endothelial dysfunction is central to pressure overload-induced cardiac hypertrophy and failure. It would be useful to clarify whether MHBFC could prevent this dysfunction. The effects of pressure overload were assessed in male Sprague-Dawley rats 6 weeks after AAB using the progression of cardiac hypertrophy to heart failure as the endpoint. The AAB-treated rats exhibited a greater progression to heart failure and had significantly elevated blood pressure, systolic and diastolic cardiac dysfunction, and evidence of left ventricular hypertrophy (LVH). LVH was characterized by increases in the ratios of heart and left ventricular weights to body weight, increased myocyte cross-sectional areas, myocardial and perivascular fibrosis, and elevated cardiac hydroxyproline. These symptoms could be prevented by treatment with MHBFC at daily oral doses of 6 and 12 mg/kg for 6 weeks. The progression to cardiac failure, which was demonstrated by increases in relative lung and right ventricular weights, cardiac function disorders and overexpression of atrial natriuretic peptide (ANP) mRNA, could also be prevented. Furthermore, MHBFC partialy rescued the downregulated nitric oxide signaling system, whereas inhibited the upregulated endothelin signaling system, normalizing the balance between these two systems. MHBFC protected the endothelium and prevented the pressure overload-induced progression of cardiac hypertrophy to cardiac failure.