Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

Zhang

et al. 2020

Euro J of Neurology

Background and purpose Acute ischaemic stroke (AIS) is a vital cause of mortality and morbidity in China. Many AIS patients develop early neurological deterioration (END). This study aimed to construct a nomogram to predict END in AIS patients. Methods Acute ischaemic stroke patients in Nanjing First Hospital were recruited as the training cohort. Additional patients in Nantong Third People’s Hospital were enrolled as the validation cohort. Multivariate logistic regression was utilized to establish the nomogram. Discrimination and calibration performance of the nomogram were tested by concordance index and calibration plots. Decision curve analysis was employed to assess the utility of the nomogram. Results In all, 1889 and 818 patients were recruited in the training and validation cohorts, respectively. Age [odds ratio (OR) 1.075; 95% confidence interval (CI) 1.059–1.091], diabetes mellitus (OR 1.673; 95% CI 1.181–2.370), atrial fibrillation (OR 3.297; 95% CI 2.005–5.421), previous antiplatelet medication (OR 0.473; 95% CI 0.301–0.744), hyper‐sensitive C‐reactive protein (OR 1.049; 95% CI 1.036–1.063) and baseline National Institutes of Health Stroke Scale (OR 1.071; 95% CI 1.045–1.098) were associated with END and incorporated in the nomogram. The concordance index was 0.826 (95% CI 0.785–0.885) and 0.798 (95% CI 0.749–0.847) in the training and validation cohorts. By decision curve analysis, the model was relevant between thresholds of 0.06 and 0.90 in the training cohort and 0.08 and 0.77 in the validation cohort. Conclusions The nomogram composed of hyper‐sensitive C‐reactive protein, age, diabetes mellitus, atrial fibrillation, previous antiplatelet medication and baseline National Institutes of Health Stroke Scale may predict the risk of END in AIS patients.

Section: Discussionmentioning

confidence: 99%

A novel nomogram to predict early neurological deterioration in patients with acute ischaemic stroke

Zhang

et al. 2020

Euro J of Neurology

“…NF-κB has been regarded as one of the most important regulatory factors of the inflammatory cascade in renal IRI as it potentially regulates post-IRI cell survival. Various studies have shown that IRI promotes the local or systemic release of pro-inflammatory cytokines, such as TNF-α and IL-6, thereby aggravating organ injury ( Wei et al, 2019 ; Farhadi Moghadam and Fereidoni, 2020 ) Farhadi Moghadam and Fereidoni, 2020 Wei et al, 2019 . Therefore, renal IRI can be alleviated by suppressing the renal ischemia-induced inflammatory response ( Kasimsetty et al, 2020 ; Zhang et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Pioglitazone Ameliorates Renal Ischemia-Reperfusion Injury via Inhibition of NF-κB Activation and Inflammation in Rats

Zou

Zhou

et al. 2021

Front. Physiol.

Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. In this study, we investigated the role of the NF-κB signaling pathway and inflammation in the amelioration of renal IRI using pioglitazone. Sprague–Dawley (SD) rats were subjected to bilateral renal artery clamping for 45 min followed by perfusion restoration for establishing a simulated renal IRI model. At 24 h post-operatively, we assessed the serum levels of creatinine and urea nitrogen, expression levels of peroxisome proliferator-activated receptor gamma (PPAR-γ) and NF-κB-related (p-IKK-β and IκB-α) proteins, and mRNA expression levels of the inflammatory cytokines, including TNF-α and MCP-1, in the renal tissue of various study groups. The histopathological evaluation of renal tissue was also conducted. In rat renal tissue, pioglitazone treatment decreased the serum levels of post-renal IRI creatinine and urea nitrogen, as well as necrosis. Furthermore, it elevated the expression of PPAR-γ protein and decreased the expression of NF-κB-related proteins. Pioglitazone also decreased the mRNA expression of TNF-α and MCP-1 in the renal tissue. Thus, pioglitazone ameliorates renal IRI by inhibiting the NF-κB signaling pathway and inflammatory response in rats.

“…These include targeted ion channels, transporters, and specific targets. Also include anti-apoptotic, anti-inflammatory, and antioxidant drugs (Tan et al, 2019 ; Moghadam and Fereidoni, 2020 ; Yang et al, 2020 ). The Sur1-Trpm4 inhibitors are of particular interest and have been studied in three clinical trials.…”

Section: Perspectivesmentioning

confidence: 99%

Potential Therapies for Cerebral Edema After Ischemic Stroke: A Mini Review

Yao

Zhang

Liao

et al. 2021

Front. Aging Neurosci.

Stroke is the leading cause of global mortality and disability. Cerebral edema and intracranial hypertension are common complications of cerebral infarction and the major causes of mortality. The formation of cerebral edema includes three stages (cytotoxic edema, ionic edema, and vasogenic edema), which involve multiple proteins and ion channels. A range of therapeutic agents that successfully target cerebral edema have been developed in animal studies, some of which have been assessed in clinical trials. Herein, we review the mechanisms of cerebral edema and the research progress of anti-edema therapies for use after ischemic stroke.