Serum Levels Of SOD Research Articles

Correlation of Glycated Hemoglobin with Oxidative Stress in Type 2 Diabetes Mellitus

Type 2 diabetes mellitus (T2DM) has a heavy disease burden and is one of the leading causes of death worldwide. It is considered to be evolving from a complex and multifactorial metabolic disorder to an inflammatory condition. The strong link between hyperglycemia and oxidative stress has long been established. Oxidative stress leads to the generation of inflammatory mediators and reactive oxygen species, which results in an inflammatory state, which plays a key role in the pathogenesis of diabetic complications. We aimed to correlate the levels of Glycated Hemoglobin with Oxidative Stress.This cross-sectional study included 200 subjects, 100 were type 2 diabetic patients and 100 were healthy non-diabetic individuals. The data were analyzed using a t test. The results showed that as the Glycated Hb increased, the levels of FBS, MDA increased and Serum SOD, Glutathione and Catalase levels decreased. The results showed a positive correlation between HbA1c and fasting blood glucose (r = 0.417, p= 0.000) and MDA (r= 0.340, p=0.000). Whereas negative correlation was observed between HbA1c and other antioxidant parameters, SOD (r= 0.025, p=0.803) Catalase (r= 0.096, p= 0.342), Glutathione (r= -0.164, p= 0.103). It is hereby concluded for the present study that when glycated Hb increases the natural antioxidants that is SOD, catalase and glutathione decrease to combact the increased formation of ROS. Serum MDA, a marker of lipid peroxidation, increased with increased glycated Hb, and shows a positive correlation, indicating that lipid peroxidation increased, when glycation of Hb increased, thus depicting an increased chance of macrovascular complication in type 2 diabetics.

Development and Validation of a Novel Diagnostic Nomogram Model Using Serum Oxidative Stress Markers and AURKA for Prediction of Nasopharyngeal Carcinoma.

The mortality rate of nasopharyngeal carcinoma (NPC) remains high due to the absence of quick and accurate diagnostic approaches at its early stage. Our aim is to evaluate the diagnostic value of the elevated expression of Aurora kinase A (AURKA) and the oxidative stress markers (such as glutathione, superoxide dismutase and malondialdehyde) in serum of NPC patients and to establish a nomogram model for predicting NPC on the ground of these biomarkers. Serum samples from 93 NPC patients and 94 healthy subjects were collected. Enzyme-linked immunosorbent assay (ELISA) was adopted to determine the AURKA level, while oxidative stress markers were measured by commercially available appropriate kits. Logistic regression was used for NPC predictor identification and nomogram construction. The training and validation cohorts (3:1) were randomly split up from the participants. Receiver operating characteristic (ROC) curves, calibration curves, and decision curve analyses (DCAs) were performed to validate the nomogram. AURKA and malondialdehyde (MDA) levels were significantly high in the NPC population compared to the healthy controls (P < 0.0001). The nomogram resulted in an area under the curve (AUC) of 0.897 (95% confidence interval: 0.848-0.947) in the training set and AUC of 0.770 (0.628-0.912) in the validation set. The predicted probability and the actual probability matched well in the nomogram (P > 0.05). DCAs showed good results too. Serum levels of AURKA, SOD, and MDA have diagnostic values in NPC. The nomogram based on the identified biomarkers is favorable for NPC prediction.

Immune response of silver pomfret (Pampus argenteus) to Photobacterium damselae subsp. Damselae: Virulence factors might induce immune escape by damaging phagosome

Photobacterium damselae subsp. damselae (PDD) is a dangerous bacterial disease that affects silver pomfret (Pampus argenteus) and its main virulence factors are pore-forming toxins. In this study, a highly pathogenic strain was obtained from naturally infected silver pomfret and was introduced into healthy fish for experimentation. Liver, gill, kidney and spleen samples were collected at 0, 24, 48, 72 and 96 h. Histopathological evaluations of these tissues, via HE staining, showed multi-organ bleeding, inflammatory infiltration and histopathocyte vacuolation as the main pathological changes. The levels of AKP, ACP, LZM, SOD, GSH and CAT in serum also displayed an increase following infection. Transcriptome sequencing of liver, kidney and spleen was performed using samples 96 h post-infection. The analysis of the resulting 770,878,120 clean reads collectively assembled into 89,310 unigenes. The WGCNA analysis demonstrated enrichment of phagosome and cytokine-cytokine receptor interaction in the liver, drug metabolism-cytochrome P450 in the kidney, and MAPK signaling pathway and other signaling pathways in the spleen. DEGs related to immune and immune-related pathways, such as Phagosome, Autophagy-animal and Glycerolipid metabolism, were significantly enriched. Selected key genes from these KEGG pathways were examined using RT-qPCR. The expression level of autophagy related genes (pi3k, bcl2) increased after infection, while the gene associated with MAPK and apoptosis (Caspase 9, mapk4) significantly increased after 72 h infection. The expression of phagosome related genes (atp6v1f, ctsl) increased initially, but later decreased. The genes related to innate immunity (ccl4, il15) were up-regulated, while those related to acquired immunity (mhc2a, mhc2b) showed a downward trend. Lysosome-related genes (gilta, giltb, cftr, c-type lectin, m6pra and m6prb) were up-regulated in liver and spleen and down-regulated in kidney and gill. The data obtained illustrated that PDD activated the immune defenses of the fish, increasing metabolic expenditure, but that the pore-forming toxins released by PDD could destroy the phagosome membrane and help the bacteria escape, which could disturb antigen presentation and inhibit the activation of the acquired immunity. This study reveals the potential immune escape mechanism of PDD in the host for the first time and has the potential to aid in the development of anti-PDD drugs.

Value of serum TGF-β1, IGF-1, MDA and SOD levels in predicting avascular necrosis of femoral head after PRP combined with internal fixation for femoral neck fracture

Value of serum TGF-β1, IGF-1, MDA and SOD levels in predicting avascular necrosis of femoral head after PRP combined with internal fixation for femoral neck fracture

Celery Ethanol Extract Prevents Renal Ischemia-Reperfusion Injury via Increasing Nitrite Oxide and Superoxide Dismutase

Background: Acute kidney injury (AKI) is one of the health problems. Kidney ischemia-reperfusion injury (IRI) contributes to pathological conditions of AKI. An imbalance between renal vasoconstriction and vasodilatation mediators was played a role in IRI and its chronic complications. Stress oxidative and inflammation were major pathomechanism of IRI. Administration of celery ethanol extract is one of the efforts to prevent kidney damage caused by IRI. This study aimed to investigate the time effect of celery ethanol extract administration on inhibition of kidney IRI. Methods: Twenty male Sprague Dawley rats with a weight range of 190-210 g were selected for the study. The rats were divided into five groups randomly: sham operation (SO, n=4) group, IRI group (ischemia-reperfusion injury, n=4), IRI+S7 (celery ethanol extract 1000 mg/kg BW 7 days orally+ischemia-reperfusion injury, n=4), IRI+S14 (celery ethanol extract 1000 mg/kg BW 14 days orally+ischemia-reperfusion injury, n=4), IRI+S28 (celery ethanol extract 1000 mg/kg BW 28 days orally+ischemia-reperfusion injury, n=4). Serum samples were collected for creatinine serum, NO, SOD, and TNF-α measurement. mRNA expression of ET-1 and ETAR was quantified using reverse transcriptase-PCR. Result: Serum creatinine, NO, and SOD level in rats with celery ethanol extract 1000 mg/kg BW for 7 and 14 days administration before IRI induction lower than IRI group (p&lt;0.05) and increase in 28 days administration. Meanwhile, the TNF-α level, ET-1, and ETAR gen expression lower than the IRI group but not significantly different (p&gt;0.05). Conclusion: Administration of celery ethanol extract 1000 mg/kg BW for 7 days and 14 days prevents renal ischemia-reperfusion injury via increasing NO and SOD. Administration more than 28 days is not recommended.

Exercise reduces hyperlipidemia-induced cardiac damage in apolipoprotein E-deficient mice via its effects against inflammation and oxidative stress

Cardiovascular disease is a high incidence and mortality rate disease worldwide. Exercise training has become an established evidence-based treatment strategy that is beneficial for many cardiovascular diseases. This study aimed to investigate the effects of exercise on hyperlipidemia-induced cardiac damage in apolipoprotein E-deficient (ApoE−/−) mice. Male ApoE−/− mice were randomly divided into the following four groups: normal diet (ND), normal diet + exercise training (ND + E), high-fat diet (HFD), and high-fat diet + exercise training (HFD + E). Exercise training consisted of swimming for 40 min, 5 days/week for 12 weeks. After 12 weeks, histopathological alterations in cardiac tissue and the serum were measured. Furthermore, the NOX4, NRF2, SIRT1, TGF-β, HO-1, collagen III, Smad3, Bax, Bak, Bcl-2, Bcl-xl, IL-1β, IL-6, and IL-18 expression levels were evaluated using immunohistochemistry and western blotting; Results: the serum levels of SIRT1, GSH-Px, and SOD were lower in ApoE−/− HFD mice compared with those in ApoE−/− HFD + E mice. Significant pathological changes were observed in the ApoE−/− HFD + E group compared with those in the ApoE−/− HFD group. Increased levels of oxidative stress, fibrosis, and apoptosis, and decreased antioxidant expression in the ApoE−/− HFD group compared with those in ApoE−/− HFD + E mice. Exercise exerts protective effects against cardiac damage caused by hyperlipidemia.

The Alleviating Impacts of Quercetin on Inflammation and Oxidant-antioxidant Imbalance in Rats with Allergic Asthma.

Asthma is an inflammatory disease of the airways. We assessed the anti-inflammatory and antioxidative impacts of quercetin, a plant derivative, on inflammatory and oxidative indices in lung tissue and serum of rats with asthma.Asth ma was induced by ovalbumin. Rats were divided into 4 groups: control, asthma+vehicle (Receieved normal saline), asthma+dexamethasone, and asthma+quercetin. After asthma induction, quercetin (50 mg/kg) and dexamethasone (2.5 mg/kg) were injected intraperitoneally once daily for 1 week. On day 50, lung histopathology indices; inflammatory factors; tissue gene expression, including GATA Binding Protein 3 (Gata-3), Tbx21 (T-bet), Transforming growth factor-β (TGF-β), Il10 (IL-10), Il1b (IL-1β), Il6 (IL-6), Acta2 (α-SMA), and Tnf (TNF-α); and oxidative stress indices (malondialdehyde [MDA], catalase [CAT], glutathioneperoxidase [GPX], superoxide dismutase [SOD], and total antioxidant capacity [TAC]) in tissue and serum, were evaluated. The results showed that quercetin reduced Gata3, Tnf, Tgfb1, Il1b, and Acta2 gene expression and increased Tbx21 gene expression following asthma. Quercetin also improved oxidative stress by decreasing MDA levels and increasing TAC, CAT, SOD, and GPX levels in serum and lung tissue. Furthermore, quercetin decreased IL6 and TNFα levels and increased IL10 levels in lung tissue after asthma was treated with quercetin. Quercetin ameliorates oxidative stress and inflammation caused by asthma, especially at the tissue level. Therefore, quercetin can be considered a potent antiasthmatic agent.

Protective effects of the Terminalia bellirica tannin-induced Nrf2/HO-1 signaling pathway in rats with high-altitude pulmonary hypertension

BackgroundOxidative stress and endothelial cell dysfunction induced by high-altitude hypoxia have important roles in the pathological process of high-altitude pulmonary hypertension (HAPH). Tannins present in Terminalia bellirica (Gaertn.) Roxb. (TTR) have pharmacological activities that produce oxidation resistance and exert anti-inflammatory effects. Whether TTR exerts a protective effect on HAPH remains unknown.MethodsA rat model of HAPH was established. The mean pulmonary arterial pressure (mPAP) of the animals was measured, the serum levels of SOD, MDA, and GSH-Px were measured using ELISA, and the expression of Bax, Bcl-2, Nrf2, and HO-1 proteins in the lung tissue of each group of rats was measured using Western blotting. Pathological changes in the lung tissue were also observed. A model of damage to H2O2-induced pulmonary artery endothelial cells (PAECs) was generated, and cell proliferation was measured using CCK-8 assays. Flow cytometry was used to measure ROS levels in PAECs. Western blotting was used to detect the expression of Bax, Bcl-2, Nrf2, and HO-1 proteins in PAECs.ResultsThe hemodynamic and pathologic findings showed that the mPAP of HAPH rats increased markedly, and the vascular wall thickness increased (P < 0.05). TTR reduced mPAP, alleviated or slowed pulmonary arterial remodeling, increased GSH-Px and SOD activity, lowered the level of MDA (P < 0.05), and downregulated the expression of Bax in the lung tissues of HAPH rats, while the expression of Bcl-2, Nrf2, and HO-1 was upregulated (P < 0.05). The results of the cell experiments showed that TTR inhibited H2O2-induced PAEC apoptosis and ROS production (P < 0.05), downregulated the expression of Bax in PAECs, and upregulated the expression of Bcl-2, Nrf2, and HO-1 (P < 0.05).ConclusionThe results suggest that TTR reduces pulmonary arterial pressure, decreases oxidative stress during HAPH, and exerts protective effects in rats with HAPH and that its mechanism of action is related to regulation of the Nrf2/HO-1 signaling pathway.

The cardioprotective effect of human glucagon-like peptide-1 receptor agonist (semaglutide) on cisplatin-induced cardiotoxicity in rats: Targeting mitochondrial functions, dynamics, biogenesis, and redox status pathways.

The cardiotoxic effect of chemotherapeutic agents as cisplatin has become a major issue recently. Interference with mitochondrial dynamics, biogenesis, redox status, and apoptosis are the most possible underlying mechanisms. Semaglutide is a human glucagon-like peptide-1 receptor agonist (GLP-1R), which is used primarily for the treatment of DM. Various recent studies have investigated (GLP-1R) role in cardiovascular diseases due to antiapoptotic and antioxidant effects. The current study aimed to investigate the curative role of semaglutide's against cisplatin- induced cardiotoxicity and its relation to mitochondrial functions, dynamics, biogenesis, apoptosis, and redox status pathways. The study included 30 male rats divided into three groups: control, cisplatin-induced cardiotoxicity, and cisplatin-induced cardiotoxicity treated with semaglutide. At the end of the experiment heart index, serum cardiotoxicity markers, SOD, GPX activities and H2 O2 level were estimated. Mitochondrial transmembrane potential, complex I and citrate synthase enzyme activities, ATP level, Mfn2 in addition to PGC-1 α levels were assessed as biogenesis markers. Mitophagy markers PINK1 and Parkin mRNA gene expression were estimated. Histopathological examination of cardiac muscles of all studied groups and immunoassay of P53 and caspase 3 in cardiac tissue were examined to assess apoptosis. Cisplatin has disturbed mitochondrial function and dynamics, dysregulate redox status and induced mitophagy and apoptosis, in the other hand semaglutide treatment has normalized dysregulated mitochondrial function and dynamics, redox status and suppressed mitophagy and apoptosis. Semaglutide has ameliorative effect against cisplatin- induced cardiotoxicity via modulation of mitochondrial functions, dynamics, biogenesis, apoptosis, and redox status pathways.

Probiotic Effects of Bacillus subtilis on Growth Performance and Intestinal Microecological Balance of Growing-to-Finishing Pigs

The present study investigated the growth performance, immune status, gut morphology, and gut microflora modulation in growing-to-finishing pigs (n = 72; 24 pigs/group) after dietary supplementation with Bacillus subtilis (B. subtilis; two groups (experiment 1 (E1) and experiment 2 (E2): 63 and 98 days, respectively) and control (Ct, basal diet). The results revealed that both 1–98 d and 1–63 d groups significantly improved growth performance, including an increase in midtest body weight (MBW) P = 0.0114 , final body weight (FBW) P &lt; 0.0001 , and average daily gain (ADG) P &lt; 0.0001 and a decrease in the ratio of feed to gain (F/G) P &lt; 0.0001 . There was an increase in serum IgG and SOD levels after supplementation with B. subtilis P = 0.0074 . Furthermore, B. subtilis potentiated the integrity of intestinal morphology (villus height (VH) P &lt; 0.0001 and villus height/crypt depth (VH/CD) P = 0.0009 ) in growing-to-finishing pigs. The LEfSe analysis identified 11 and 13 biomarkers in the fecal samples of the 1–63 d group and 1–98 d, respectively. The gut microflora alterations of growth-finishing pigs suggested that dietary B. subtilis could promote gut health by altering the relative abundances of different bacterial communities. A correlation analysis showed that B. subtilis could regulate the functional network of the intestine microflora and their interactions with its host. Taken together, dietary B. subtilis supplementation had a positive influence on the growth performance, gut health, and the composition of gut microorganisms, suggesting that B. subtilis can be used as a functional probiotic candidate for application in the production of growing-to-finishing pigs. Practical Applications. The addition of probiotics in the diet can modulate intestinal health, improve the digestibility of nutrients, and thus, help improve the nutrient utilization and production performance of pigs. It is one of the ideal substitutes for antibiotics. This study will help us understand the function of B. subtilis in the regulation of pig intestinal health, so as to provide scientific basis for the rational use of probiotics in the future pig industry.

LEVELS OF ENZYMATIC ANTIOXIDANT SUPEROXIDE DISMUTASE AND NONENZYMATIC ANTIOXIDANT URIC ACID IN POLYCYSTIC OVARY SYNDROME PATIENTS IN A TERTIARY CARE HOSPITAL OF ASSAM

Background: Polycystic ovary syndrome (PCOS) is one of the most common hormonal disorders, occurring in 5–10% women in reproductive ages. Despite a long history of studies on PCOS, its aetiology is still unknown. Oxidative stress is now recognized to play a central role in the pathophysiology of many different disorders, including PCOS. Although intracellular reactive oxygen species (ROS) production and propagation are controlled by highly complex antioxidant enzymatic and non-enzymatic systems, understanding of mechanisms that oxidative stress is important to develop strategies for prevention and treatment of PCOS. Objectives: To estimate the serum levels of superoxide dismutase and uric acid in PCOS patients. Methodology:Acase-control study was conducted in a tertiary care hospital of Assam, with 60 PCOS patients attending the outpatient Department of Obstetrics and Gynaecology, Gauhati Medical College and Hospital (GMCH), Guwahati, Assam along with 60 healthy controls of same age group. The samples were evaluated by ELISA and VITROS 5600 Autoanalyser using standard kits and reagents in the Department of Biochemistry, GMCH. Results: The results were statistically analysed and the mean and SD of SOD were found to be 969.95 + 62.96 among the cases and 1298.8 + 137.8 among the controls with p value &lt;0.001, whereas the mean and SD of uric acid was 5.41 + 0.70 in cases and 3.76 + 0.74 in controls with p value &lt;0.001.Conclusions: Signicantly lower serum levels of SOD and signicantly higher levels of Uric acid were found in cases with PCOS compared to the control group.

Hormonal and inflammatory modulatory effects of hesperidin in hyperthyroidism-modeled rats.

The goal of the current study was to investigate the hormonal modulatory efficiency of hesperidin, through its regulatory potential of immunological, inflammatory, and/or antioxidant changes in on hyperthyroidism modeled adult female albino rats. Both normal and hyperthyroidism modeled rats (140-160g) were randomly divided into four groups (10 animals each) as follows: 1) healthy animals were daily ingested with saline for six weeks, and served as control group, 2) healthy animals were intraperitoneally injected with hesperidin (50 mg/kg/day) for a similar period, 3) hyperthyroidism-modeled animals without any treatment acted as positive control, and 4) hyperthyroidism-modeled animals were treated intraperitoneally with hesperidin for a similar period. The findings showed that hesperidin significantly modulated hyperthyroidism deteriorations, this was evidenced by a remarkable decline in serum T4, FT4, T3, FT3, TNF-α, IL1β-, IL4-, IL-6, and IL-10 levels, with a minor increase in TSH and significant raise in CD4+ level. Similarly, valuable improvement was observed in the oxidative status; serum SOD, GPx, CAT, and GSH levels were dramatically enhanced, associated with remarkable drop in MDA and NO levels. Also, hesperidin demonstrated nephro-hepatoprotective and anti-atherogenic potential, this was achieved from the notable reduction in ALAT and ASAT activities as well as urea, creatinine, cholesterol, and triglyceride close to the corresponding values of healthy group. These findings were supported by histological and immunohistochemical ones that showed a notable decrease in the expression of the calcitonin antibody. In conclusion, hesperidin possesses anti-hyperthyroidism, immunoinflammatory regulatory, and antioxidant activities that evidenced from the improvement of physio-architecture of the thyroid gland, reduction of inflammation and restoration of the impaired oxidative stress. This effect might be mechanized through immunological, inflammatory, apoptotic, and/or antioxidant modulatory pathways.

Effect of aqueous extract of Asparagus officinalis on some Antioxidants in Rats Exposed to Oxidative Stress induced by Hydrogen peroxide

The current study dealt with using of hydrogen peroxide with 0.5% with drinking water to induce state of oxidative stress in male rats and estimate the ability of different concentrations of the aqueous extract of asparagus officinalis to reduce the effects of oxidative stress during periods 0,15,30 days by measuring the following parameters in serum: Glutathione(GSH), Malondialdehyde (MDA), the activity of super oxide dismutase enzyme (SOD) and the peroxynitrate radical (ONOO).&#x0D; Fifty male rats with the age of 3-4 months and weight of 300-400 gm were distributed into 5 groups: group (1): control group received drinking tap water, group (2): treated with H2O2 0.5% in drinking water, group (3): treated with H2O2 and asparagus officinalis 5%, group (4): treated with H2O2 and asparagus officinalis 10%, group (5): treated with H2O2 and asparagus officinalis 20% . Hydrogen peroxide treatment led to a significant decrease (P &lt;0.05) of the GSH and SOD activities and increase of the MDA and ONOO levels in the serum during treatment periods compared with the control group. The results of using different concentrations of aqueous extract of asparagus on rats revealed similar effects but not identical in the protection from the oxidative stress induced by Hydrogen Peroxide , because its effect was affected on the level of GSH, SOD, MDA and ONOO levels in the blood serum in different experiment period.

The Mechanisms of Neochlorogenic Acid (3-Caffeoylquinic Acid) in Improving glucose and Lipid Metabolism in Rats with Insulin Resistance Induced by A High Fat-High Fructose Diet

This study investigated the effects and the mechanism of actions of neochlorogenic acid (3-caffeoylquinic acid; 3-CQA) on glucose and lipid metabolism in rats fed a high fat-high fructose diet (HFFD). Male rats were fed HFFD (40 % lard and 20 % fructose) for 16 weeks. At the 10th week, the HFFD rats were split into 3 groups: HFFD receiving distilled water (HFFD control group), HFFD receiving 3-CQA 50 mg/kg and HFFD receiving metformin 200 mg/kg once daily for a further 6 weeks. At the end of treatment, fasting blood glucose (FBG), oral glucose-tolerance test (OGTT), lipid profile, insulin, leptin, adiponectin, markers of oxidative stress, and hepatic triglyceride content were measured. Liver, adipose tissue, and skeletal muscle were collected for histological, gene and protein examinations. Compared to the HFFD control group, the 3-CQA group exhibited significantly reduced FBG, insulin and leptin levels, and improved OGTT. Serum adiponectin increased and lipid profiles were normalized. Hepatic triglyceride was reduced with a decrease in lipid droplets in liver histological sections. Levels of serum SOD and CAT activity, and MDA were reversed by 3-CQA treatment. Moreover, 3-CQA significantly reduced the expression of adipocyte pro-inflammatory cytokine genes (MCP-1, TNF-α, and IL-6), hepatic lipogenic genes (SREBP1c, FAS, and GPAT), and hepatic gluconeogenic genes (PEPCK and G6Pase). Additionally, 3-CQA increased expression of muscle GLUT4 gene, and of GLUT4 protein with increased p-AKT and p-AMPK in skeletal muscle. In conclusion, 3-CQA improves glucose and lipid metabolism plausibly by decreasing oxidative stress and inflammation-induced insulin resistance, downregulating the expression of lipogenic and gluconeogenic genes, and enhancing insulin signaling in HFFD-induced insulin-resistant rats. HIGHLIGHTS Neochlorogenic acid (3-CQA) improves glucose and lipid metabolism by decreasing insulin resistance Neochlorogenic acid (3-CQA) deceases insulin resistance due to its activities in ameliorating obesity, oxidative stress, and adipose tissue inflammation The beneficial effects of Neochlorogenic acid (3-CQA) to improve glucose and lipid homeostasis may be mediated via suppression of hepatic glucose production and lipogenesis, and activation of muscle glucose uptake and AKT and AMPK pathways GRAPHICAL ABSTRACT

Cuproptosis is involved in copper-induced hepatotoxicity in chickens

Copper (Cu) is an essential trace element, but it is also a ubiquitous environmental pollutant that threatens public health. Cuproptosis is a recently discovered cell death mode that unlike other programmed cell death, characterized by proteotoxic stress due to lipoylated protein aggregation and iron-sulfur cluster protein loss. Chickens as a high-trophic-level non-mammalian vertebrate that easily absorb and accumulate copper from the environment and food, but it is unclear whether the underlying molecular mechanisms that cause their hepatotoxicity under natural copper stress are related to cuproptosis. Therefore, we established animal models of chickens with different concentrations of copper exposure to dissect the role and mechanism of cuproptosis in chicken hepatotoxicity under natural copper stress. Our histopathological and biochemical results demonstrated that the liver structure with copper-treated exhibited dose-dependent damage. Meanwhile, copper treatment also dramatically increased serum and liver copper content and activated the expression of the membrane-associated copper transporter ATP7B. Furthermore, we found that Cu-exposure significantly increased the MDA content, and reduced the levels of T-AOC and SOD in serum and liver. Additionally, we found that the mRNA and protein levels of FDX1 were significantly upregulated in the 220 and 330 mg/kg Cu-treated groups. In our further studies, we found that copper did not alter protein levels of DLAT and DLST in chicken liver, but significantly increased Lipoylated-DLAT levels and oligomerization of Lipoylated-DLAT in the 330 mg/kg Cu-treatment group. Overall, we identified that FDX1-mediated protein lipoylation and proteotoxic stress indeed participate in copper-induced hepatotoxicity in chickens. Our results present novel insight into the pathogenesis of copper-induced hepatotoxicity in chickens and provide data to support filling in the role of cuproptosis in birds.

Effects of electroacupuncture combined with acupoint catgut embedding on gastrointestinal motility and gastrointestinal hormones in rats with functional dyspepsia.

Electroacupuncture (EA) or acupoint catgut embedding (ACE) plays a therapeutic role in functional dyspepsia (FD). Herein, we aimed to elucidate the influences of EA combined with ACE on gastrointestinal motility and gastrointestinal hormones in rats with FD. Sprague-Dawley rats were randomized into the control group, model group, EA group, ACE group, and EA + ACE group (n = 10). Except for the control group, the rats in all groups were modeled by combining neonatal iodoacetamide gastrogavage and modified tail-clamping stimulation. The rats were treated with different treatments according to their groups. The rats were observed for changes in general behavior, body weight, food intake, and paw mechanical pain threshold. Gastric emptying rate (GER) and intestinal propulsive ratio (IPR) were measured in each group, and serum gastrointestinal hormone (motilin [MTL], leptin, gastrin [GAS], vasoactive intestinal peptide [VIP], calcitonin gene-related peptide [CGRP], and somatostatin [SS]) levels, oxidative stress factors (superoxide dismutase [SOD] and malondialdehyde [MDA]) and 5-hydroxytryptamine (5-HT) levels were also measured. Decreased mean body weight, paw mechanical pain thresholds, food intake, and GER and IPR were found in rats of the model group in comparison to the control group. Serum MTL, GAS, SS, and SOD levels were reduced, and serum leptin, VIP, CGRP, MDA, and 5-HT levels were increased in rats of the model group in comparison to the control group. Elevated mean body weight, paw mechanical pain threshold, food intake, GER and IPR, and serum MTL, GAS, SS, and SOD levels, and reduced serum leptin, VIP, CGRP, MDA, and 5-HT levels were observed in rats of the EA, ACE, and EA + ACE groups relative to the model group. EA combined with ACE treatment was more effective than the EA or ACE treatment alone. EA combined with ACE treatment improves gastrointestinal motility and gastrointestinal hormone levels, promotes food intake, and reduces visceral hypersensitivity in FD rats.

Improvement effect of enzymic polypeptide from Paeonia ostii seed meal on protein-energy malnutrition mouse model

The improvement effects of enzymatic polypeptide of Paeonia ostii seed meal (APHP) on model mice of protein-energy malnutrition were evaluated by body weight changes, organ indices, levels of SOD, CAT, MDA, total protein and albumin in serum, staining images of major organs and macrophages phagocytosis. The results indicated the mice body weight recovery was dose-dependent with APHP and the body weight change of model mice fed with high-dose APHP (5.0 g/kg) and normal diet showed a same recovery effect. The model mice had higher thymus and spleen indexes than other groups. And the values of SOD, CAT, MDA, total protein and albumin in serum returned to normal level after 30, 60, 45, 30 and 45 days respectively, which was better than those of normal diet. Our research will provide basic data support for new potential applications of APHP and increase the added value of Paeonia ostii processing enterprises.

Serum ANGPTL4 and FGF2, energy-related blood biochemicals, cytokine responses and oxidative stress in dairy cows with subclinical ketosis

In this study, it was aimed to investigate the serum levels of ANGPTL4, FGF21, IL-1β, IL-6, SOD, MDA, and serum biochemical and hematological parameters in cows with subclinical ketosis. The mean serum β-hydroxybutyric acid (BHB) level was 1.37 ± 0.04 mmol/L in 10 dairy cows aged 3-5 years that were &amp;lt;21 days postpartum and diagnosed with subclinical ketosis. The mean serum BHB level was 0.40 ± 0.08 mmol/L in 10 healthy dairy cows in the same period and in the same age range. An increase in serum AST (P&amp;lt;0.001) and a decrease in serum albumin levels (P&amp;lt;0.05) indicated altered liver functions. An increase in serum non-esterified fatty acid (P&amp;lt;0.001) and decreases in serum HDL, triglyceride, and total cholesterol levels (P&amp;lt;0.05) were interpreted as indicators of increased metabolic pathology risk due to negative energy balance. Increases in serum ANGPTL4, FGF2, IL-1β, IL-6, and MDA (P&amp;lt;0.001) and SOD levels (P&amp;lt;0.05) were evaluated as indicators of the development of effective metabolic, inflammatory, and oxidative stress.It was concluded that significant increases in serum ANGPTL4, FGF2, IL-1β, IL-6, and MDA and SOD levels in dairy cows with subclinical ketosis were associated with negative energy balance, effective cytokine responses, and oxidative stress.

Cardioprotective Effects of Aconite in Isoproterenol-Induced Myocardial Infarction in Rats.

Myocardial infarction (MI) is a severe clinical condition caused by decreased or complete cessation of blood flow to a portion of the myocardium. Aconite, the lateral roots of Aconitum carmichaelii Debx., is a well-known Chinese medicine for treatment of heart failure and related cardiac diseases. The present study is aimed at investigating the cardioprotective effect of aconite on isoproterenol- (ISO)- induced MI. The qualitative analysis of aqueous extracts from brained aconite (AEBA) was conducted by HPLC. A rat model of MI induced by ISO was established to examine the effects of AEBA. The cardiac function was assessed by echocardiography. The serum levels of SOD, CK-MB, cTnT, and cTnI were detected to estimate myocardial injury. The pathological changes of heart tissue were evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) staining, hematoxylin-eosin (HE) staining, and Masson's trichrome staining. The expressions of abnormal vascular remodeling and hypoxia-related components and the levels of inflammation-associated genes and proteins were detected by RT-qPCR, western blotting, and immunofluorescence. The contents of benzoylaconine, benzoylmesaconine, benzoylhypacoitine, and hypaconitine in AEBA were 1.35 μg/g, 37.35 μg/g, 57.10 μg/g, and 2.46 μg/g, respectively. AEBA obviously improved heart function through promoting echocardiographic parameters, radial strain, and circumferential strain. The data of TTC staining, HE staining, and Masson's trichrome staining disclosed that AEBA could significantly reduce infarct size, inhibit inflammatory cell infiltration, and decrease the myocardial fibrosis. Moreover, AEBA distinctly suppressed the serum levels of SOD, MDA, CK-MB, cTnT, and cTnI in ISO-induced rats. The results of RT-qPCR indicated that AEBA inhibited the expressions of hypoxia- and inflammation-related genes, including VEGF, PKM2, GLUT-1, LDHA, TNF-α, IL-1β, IL-6, and COX2. In addition, the western blotting and immunofluorescence analyses further confirmed the results of RT-qPCR. In summary, our results indicate that the AEBA could improve ISO-induced myocardial infarction by promoting cardiac function, alleviating myocardial hypoxia, and inhibiting inflammatory response and fibrosis in heart tissue.

Serum and brain metabolomic study reveals the protective effects of Bai-Mi-Decoction on rats with ischemic stroke.

Bai-Mi-Decoction (BMD), which is composed of Eugenia caryophyllata, Myristica fragrans, Moschus berezovskii, and Crocus sativu, is a characteristic TCM multi-herb formula for brain disease. However, the mechanism of protective effects of BMD on ischemic stroke (IS) still has not been clarified. Our study is designed to elucidate the protective effects and underlying mechanisms of BMD on IS by employing pharmacodynamic and serum and brain metabolomic methods. In this experiment, 90 adult male Sprague-Dawley rats were randomly divided into the sham operation group (SHAM, vehicle), middle cerebral artery occlusion-reperfusion injury model group (MCAO/R, vehicle), positive control group (NMDP, 36mg/kg/day nimodipine), and low (BMDL, 0.805g/kg/day), moderate (BMDM, 1.61g/kg/day), and high (BMDH, 3.22g/kg/day) dosage of BMD prophylactic administration groups. The drugs were dissolved in 0.5% CMC-Na and orally administered to rats with equal volumes (100g/ml body weight) once a day for 14 consecutive days. Neurological deficit score, cerebral infarct volume, change in body weight, and serum NO, SOD, MDA, GSH, and GSSG levels were determined. Pathological abnormalities using hematoxylin and eosin staining and the expression of VEGF, caspase-3, and NF-κB were analyzed. Furthermore, serum and brain metabolic profiles were explored to reveal the underlying mechanism using UHPLC-QTOF-MS/MS technology. BMD exhibited significant neuroprotective effects on MCAO/R rats. As compared to the MCAO/R model group, it could reduce the neurological deficit score and cerebral infarct volume, increase body weight, enhance GSH, SOD, and GSSG activities, and decrease NO and MDA contents of MCAO/R rats. Meanwhile, BMD could ameliorate pathological abnormalities of MCAO/R rats through reducing neuronal loss, vacuolated spaces, shrunken neurons, and destructed neuron structure, as well as regulating the expression of VEGF, caspase-3, and NF-κB. UHPLC-QTOF-MS/MS-based serum and brain metabolomics analysis found a total of 53 differential metabolites between MCAO/R and SHAM groups, of which 30 were significantly regulated by BMD intervention, and further metabolic pathway analysis implied that the protective effects were mainly associated with amino acid and glycerophospholipid metabolisms. Our pharmacodynamic and metabolomic results revealed the neuroprotective effects of BMD on MCAO/R rats, and the underlying mechanisms were probably related to amino acid and glycerophospholipid metabolisms.