10 research outputs found
Hypertension as a sequela in patients of SARS-CoV-2 infection.
BACKGROUND: COVID-19 is a respiratory infectious disease caused by SARS-CoV-2, and cardiovascular damage is commonly observed in affected patients. We sought to investigate the effect of SARS-CoV-2 infection on cardiac injury and hypertension during the current coronavirus pandemic.
STUDY DESIGN AND METHODS: The clinical data of 366 hospitalized COVID-19-confirmed patients were analyzed. The clinical signs and laboratory findings were extracted from electronic medical records. Two independent, experienced clinicians reviewed and analyzed the data.
RESULTS: Cardiac injury was found in 11.19% (30/268) of enrolled patients. 93.33% (28/30) of cardiac injury cases were in the severe group. The laboratory findings indicated that white blood cells, neutrophils, procalcitonin, C-reactive protein, lactate, and lactic dehydrogenase were positively associated with cardiac injury marker. Compared with healthy controls, the 190 patients without prior hypertension have higher AngⅡ level, of which 16 (8.42%) patients had a rise in blood pressure to the diagnostic criteria of hypertension during hospitalization, with a significantly increased level of the cTnI, procalcitonin, angiotensin-II (AngⅡ) than those normal blood pressure ones. Multivariate analysis indicated that elevated age, cTnI, the history of hypertension, and diabetes were independent predictors for illness severity. The predictive model, based on the four parameters and gender, has a good ability to identify the clinical severity of COVID-19 in hospitalized patients (area under the curve: 0.932, sensitivity: 98.67%, specificity: 75.68%).
CONCLUSION: Hypertension, sometimes accompanied by elevated cTnI, may occur in COVID-19 patients and become a sequela. Enhancing Ang II signaling, driven by SARS-CoV-2 infection, might play an important role in the renin-angiotensin system, and consequently lead to the development of hypertension in COVID-19
Effects of S-adenosylmethionine on liver methionine metabolism and steatosis with ethanol-induced liver injury in rats
The Beneficial Roles of SIRT1 in Neuroinflammation-Related Diseases
Sirtuins are the class III of histone deacetylases whose deacetylate of histones is dependent on nicotinamide adenine dinucleotide (NAD+). Among seven sirtuins, SIRT1 plays a critical role in modulating a wide range of physiological processes, including apoptosis, DNA repair, inflammatory response, metabolism, cancer, and stress. Neuroinflammation is associated with many neurological diseases, including ischemic stroke, bacterial infections, traumatic brain injury, Alzheimer’s disease (AD), and Parkinson’s disease (PD). Recently, numerous studies indicate the protective effects of SIRT1 in neuroinflammation-related diseases. Here, we review the latest progress regarding the anti-inflammatory and neuroprotective effects of SIRT1. First, we introduce the structure, catalytic mechanism, and functions of SIRT1. Next, we discuss the molecular mechanisms of SIRT1 in the regulation of neuroinflammation. Finally, we analyze the mechanisms and effects of SIRT1 in several common neuroinflammation-associated diseases, such as cerebral ischemia, traumatic brain injury, spinal cord injury, AD, and PD. Taken together, this information implies that SIRT1 may serve as a promising therapeutic target for the treatment of neuroinflammation-associated disorders
HDAC2 inhibitor CAY10683 reduces intestinal epithelial cell apoptosis by inhibiting mitochondrial apoptosis pathway in acute liver failure
Introduction. Histone deacetylases (HDAC)
inhibitor has the effect of anti-tumor and inhibiting
apoptosis, and could inhibit the release of inflammatory
factors, reducing the damage to liver and enterocytes in
acute liver failure (ALF). HDAC2 specific inhibitor
CAY10683 was used to verify the protective effect on
acute liver failure through reducing intestinal epithelial
cell apoptosis by inhibiting mitochondrial apoptosis
pathway. Materials and methods. Lipopolysaccharide/D-
galactosamine (LPS/D-GalN) was used to induce ALF in
Sprague-Dawley rats. A total of 18 healthy rats were
randomly divided into three groups. Rats in ALF group
and CAY10683 group were given the same amount of
normal sodium or CAY10683 2 hours before ALF model
protocol was conducted. NCM460 cells were given
LPS/D-GalN to establish an apoptotic model. Flow
cytometry analysis was used to determine the apoptosis
of enterocytes, and TUNEL assay was used to observe
the apoptosis of NCM460 cells. The expression of bax
was observed by immunofluorescence. The expression
of histone proteins, HDAC2 and molecules in the
apoptotic signaling pathway were determined by
Western blotting and real-time PCR. Results. CAY10683
improves histological and functional changes in ALF
model. Compared with control group, LPS/D-GalN
induced massive apoptosis of rat intestinal tissues and
NCM460 cells (P<0.05), and the apoptosis rate was
significantly reduced after CAY10683 treatment
(P<0.05). The expression of bax was increased
significantly in the model groups (P<0.05), and reduced
with the treatment of CAY10683 (P<0.05). Compared
with the model group, CAY10683 inhibits mitochondrial
apoptosis in intestinal tissues and NCM460 cells
(P<0.05). Conclusion. CAY10683 reduces the damage to
liver and intestinal tissue, and plays an important role in
inhibiting mitochondrial apoptosis in ALF rats and in
NCM460 cell
Epigallocatechin-3-gallate ameliorates alcohol-induced liver injury in rats
Abstract: Endotoxemia is a common event in alcoholic liver disease. Elevated intestinal permeability is the major factor involved in the mechanism of alcoholic endotoxemia and the pathogenesis of alcoholic liver disease. This study examined the effect of epigallocatechin-3-gallate (EGCG) on alcohol-induced gut leakiness, and explored the related mechanisms involved in its protection against alcohol-induced liver injury in rats. Four groups of female Sprague-Dawley rats were studied. Alcohol and alcohol/EGCG groups rats received fish oil along with alcohol daily via gastrogavage for 6 weeks, and dextrose and dextrose/EGCG groups rats were given fish oil along with isocaloric dextrose instead of alcohol. The dextrose/EGCG and alcohol/EGCG groups received additional treatment of EGCG (100mg.kg-1 body weight) daily intragastrically by gavage. Intestinal permeability was assessed by urinary excretion of lactulose and mannitol (L/M ratio). Liver injury was evaluated histologically and by serum alanine aminotransferase (ALT). Plasma endotoxin and serum tumor necrosis factor-α (TNF-α) levels were assayed; liver malondialdehyde (MDA) contents determined. CD14 and inflammatory factors, such as TNF-α, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) mRNAs i
Histone deacetylase 6 inhibitor ACY1215 ameliorates mitochondrial dynamic and function injury in hepatocytes by activating AMPK signaling pathway in acute liver failure mice
Acute liver failure (ALF) is often
accompanied by dynamic and functional disorders of
mitochondria in hepatocytes. The histone deacetylase 6
inhibitor Rocilinostat (ACY1215) has a hepatoprotective
effect. However, its protective effect on mitochondria of
hepatocytes and its related mechanisms in ALF remain
unknown. The purpose of the present study was to
elucidate the protective effect of ACY1215 on
mitochondrial of hepatocytes in ALF by regulating
AMPK signaling pathway. LPS and D-Gal were used to
induce ALF model in C57BL/6 mice. D-Gal and TNF-α
were applied in L02 cells as model group. ACY1215
was administered to the mice or culture cells before the
model' s establishment as ACY1215 group. The normal
group in mice and L02 cells was not given any drug
intervention. ACY1215 improves liver histological and
functional changes in ALF model mice. Compared with
normal group, the expression of p-AMPK and p-ACC
proteins was decreased in model group. ACY1215
activated the AMPK signaling pathway with an increase
of p-AMPK and p-ACC proteins level in model group.
ACY1215 treatment decreased levels of mitochondrial
fission proteins DRP1 and FIS1, and enhanced levels of
mitochondrial fusion proteins MFN1, MFN2 and OPA1
in models. MtDNA copies in model group was decreased
compared with normal group, but ACY1215 elevated the
mtDNA copies in models. Mitochondrial respiratory
electron transfer chain Complex I-III and citrate
synthase (CS) activities in model group were decreased
compared with normal group, but ACY1215 treatment
enhanced these activities in model group. ACY1215
protects against dynamic disorders and dysfunction of
mitochondria in hepatocytes in ALF by activating
AMPK signaling pathway
Clinical characteristics of 25 death cases with COVID-19: a retrospective review of medical records in a single medical center, Wuhan, China
OBJECTIVES: This study aims to summarize the clinical characteristics of death cases with COVID-19 and to identify critically ill patients of COVID-19 early and reduce their mortality.
METHODS: The clinical records, laboratory findings and radiological assessments included chest X-ray or computed tomography were extracted from electronic medical records of 25 died patients with COVID-19 in Renmin Hospital of Wuhan University from Jan 14 to Feb 13, 2020. Two experienced clinicians reviewed and abstracted the data. RESULTS: The age and underlying diseases (hypertension, diabetes, etc.) were the most important risk factors for death of COVID-19 pneumonia. Bacterial infections may play an important role in promoting the death of patients. Malnutrition was common to severe patients. Multiple organ dysfunction can be observed, the most common organ damage was lung, followed by heart, kidney and liver. The rising of neutrophils, SAA, PCT, CRP, cTnI, D-dimer, LDH and lactate levels can be used as indicators of disease progression, as well as the decline of lymphocytes counts. CONCLUSIONS: The clinical characteristics of 25 death cases with COVID-19 we summarized, which would be helpful to identify critically ill patients of COVID-19 early and reduce their mortality