scholarly journals Protective Effects of Inflammation of Curcumae Longae Rhizoma 30% EtOH Extract on Acute Reflux Esophagitis Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Jin A. Lee ◽  
Mi-Rae Shin ◽  
Min Ju Kim ◽  
Ji Hye Lee ◽  
Hae-Jin Park ◽  
...  
Keyword(s):  
Reflux Esophagitis ◽  
Stomach Contents ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Related Factors ◽  
Etoh Extract

Gastroesophageal reflux disease (GERD) is induced by the reflux of stomach contents or gastric acid, pepsin into the esophagus for prolonged periods of time due to defection of the lower esophageal sphincter. Reflux esophagitis is a disease found in less than 50% of GERD patients. This study is aimed at evaluating the protective effect of Curcumae longae Rhizoma 30% EtOH extract (CLR) in acute reflux esophagitis (ARE) rats. CLR measured antioxidant activity through in vitro experiments. Based on the results, we performed experiments in vivo. Before 90 min ARE induction, CLR was administered orally by concentration. ARE was derived by linking the metastatic junction between pylorus and forestomach and corpus in Sprague-Dawley rats. And rats were sacrificed 5 h after surgery. We analyzed the expression of antioxidant and inflammatory-related markers by western blot and observed the production of alanine aminotransferase (ALT), aspartate aminotransferase (AST), reactive oxygen species (ROS), peroxynitrite (ONOO-), and thiobarbituric acid reactive substance (TBARS). The administration of CLR reduced esophagus tissue damage in rats with acute reflux esophagitis and decreased the elevated ALT, AST, ROS, ONOO-, and TBARS. In addition, CLR effectively increased antioxidant-related factors and reduced inflammatory protein. Overall, these results suggest that CLR would be used as a therapeutic material in protection and treatment for ARE. Overall, CLR treatment informed that markedly ameliorated inactivation of NF-κB led to the inhibition of the expressions of proinflammatory proteins. These results suggest that CLR would be used as a therapeutic material in protection and treatment for ARE.

scholarly journals Evaluation of theIn VitroandIn VivoAntioxidant Potentials ofSudarshanaPowder

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Weerakoon Achchige Selvi Saroja Weerakoon ◽  
Pathirage Kamal Perera ◽  
Dulani Gunasekera ◽  
Thusharie Sugandhika Suresh
Keyword(s):  
Antioxidant Activity ◽  
Antioxidant Capacity ◽  
Thiobarbituric Acid ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Trolox Equivalent ◽  
Antioxidant Effects

Sudarshanapowder (SP) is one of the most effective Ayurveda powder preparations for paediatric febrile conditions. The objective of the present study was to evaluate thein vitroandin vivoantioxidant potentials of SP. Thein vitroantioxidant effects were evaluated using ABTS radical cation decolourization assay where the TROLOX equivalent antioxidant capacity (TEAC) was determined. Thein vivoantioxidant activity of SP was determined in Wistar rats using the Lipid Peroxidation (LPO) assay in serum. Thein vitroassay was referred to as the TROLOX equivalent antioxidant capacity (TEAC) assay. For thein vivoassay, animals were dosed for 21 consecutive days and blood was drawn to evaluate the MDA level. Thein vitroantioxidant activity of 0.5 μg of SP was equivalent to 14.45 μg of standard TROLOX. The percentage inhibition against the radical formation was50.93±0.53%. The SP showed a statistically significant (p<0.01) decrease in the serum level of thiobarbituric acid-reactive substance in the test rats when compared with the control group. These findings suggest that the SP possesses potent antioxidant activity which may be responsible for some of its reported bioactivities.

Oxidation of olive oil fortified with quercetin, caffeic acid, tyrosol and hydroxytyrosol

2015 ◽  
Vol 45 (3) ◽  
pp. 493-508 ◽  
Author(s):  
Anne Kristine Etherton ◽  
Stanley T. Omaye
Keyword(s):  
Olive Oil ◽  
Caffeic Acid ◽  
Thiobarbituric Acid ◽  
Monounsaturated Fatty Acids ◽  
Polyphenolic Compounds ◽  
Thiobarbituric Acid Reactive Substance ◽  
Content Type ◽  
Health Promoting

Purpose – This paper aims to evaluate effects of the fortification of polyphenolic compound mixtures of quercetin, caffeic acid, tryrosol and hydroxytyrosol in olive oil oxidation. Design/methodology/approach – The authors measured olive oxidation initiated by copper using thiobarbituric acid reactive substance, as an indicator of lipid peroxidation. Findings – Overall, most mixture combinations exhibited oxidation similar to olive oil alone. Some mixture combinations of polyphenolic compounds acted as antioxidants; however, as the concentrations were changed, they became prooxidant in nature. Research limitations/implications – In vitro studies have limitations for extrapolation to in vivo and clinical studies. Practical implications – Such information will be useful in determining optimal concentrations and combinations of antioxidants for reducing rancidity and perhaps as models that could be used to modulate various chronic diseases that are associated with oxidative stress. Originality/value – Olive oil, along with fruits, vegetables and fish, are important constituents of health promoting diets, such as the Mediterranean diet. Active ingredients include monounsaturated fatty acids, oleic acid and a variety of antioxidants including various polyphenolic compounds.

scholarly journals Inhibition of gap junction composed of Cx43 prevents against acute kidney injury following liver transplantation

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Dongdong Yuan ◽  
Xiaoyun Li ◽  
Chenfang Luo ◽  
Xianlong Li ◽  
Nan Cheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Transplantation ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Organ Protection ◽  
Cx43 Expression

Abstract Postoperative acute kidney injury (AKI) is a severe complication after liver transplantation (LT). Its deterioration and magnification lead to the increase in mortality. Connexin43 (Cx43) mediates direct transmission of intracellular signals between neighboring cells, always considered to be the potent biological basis of organ damage deterioration and magnification. Thus, we explored the effects of Cx43 on AKI following LT and its related possible mechanism. In this study, alternations of Cx43 expression were observed in 82 patients, receiving the first-time orthotopic LT. We built autologous orthotopic liver transplantation (AOLT) models with Sprague–Dawley (SD) rats in vivo, and hypoxia-reoxygenation (H/R) or lipopolysaccharide (LPS) pretreatment models with kidney tubular epithelial cells (NRK-52E) in vitro, both of which were the most important independent risk factors of AKI following LT. Then, different methods were used to alter the function of Cx43 channels to determine its protective effects on AKI. The results indicated that patients with AKI suffering from longer time of tracheal intubation or intensive care unit stay, importantly, had significantly lower survival rate at postoperative 30 days and 3 years. In rat AOLT models, as Cx43 was inhibited with heptanol, postoperative AKI was attenuated significantly. In vitro experiments, downregulation of Cx43 with selective inhibitors, or siRNA protected against post-hypoxic NRK-52E cell injuries caused by H/R and/or LPS, while upregulation of Cx43 exacerbated the above-mentioned cell injuries. Of note, alternation of Cx43 function regulated the content of reactive oxygen species (ROS), which not only mediated oxidative stress and inflammation reactions effectively, but also regulated necroptosis. Therefore, we concluded that Cx43 inhibition protected against AKI following LT through attenuating ROS transmission between the neighboring cells. ROS alternation depressed oxidative stress and inflammation reaction, which ultimately reduced necroptosis. This might offer new insights for targeted intervention for organ protection in LT, or even in other major surgeries.

scholarly journals NAD+ improves cognitive function and reduces neuroinflammation by ameliorating mitochondrial damage and decreasing ROS production in chronic cerebral hypoperfusion models through Sirt1/PGC-1α pathway

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Yao Zhao ◽  
Jiawei Zhang ◽  
Yaling Zheng ◽  
Yaxuan Zhang ◽  
Xiao Jie Zhang ◽  
...  
Keyword(s):  
Mitochondrial Damage ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Ros Production ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Mechanistic Pathway ◽  
Bv2 Microglia

Abstract Background Microglial-mediated neuroinflammation plays an important role in vascular dementia, and modulating neuroinflammation has emerged as a promising treatment target. Nicotinamide adenine dinucleotide (NAD+) shows anti-inflammatory and anti-oxidant effects in many neurodegenerative disease models, but its role in the chronic cerebral hypoperfusion (CCH) is still unclear. Methods The bilateral common carotid artery occlusion (BCCAO) was performed to establish CCH models in Sprague-Dawley rats. The rats were given daily intraperitoneal injection of NAD+ for 8 weeks. The behavioral test and markers for neuronal death and neuroinflammation were analyzed. Mitochondrial damage and ROS production in microglia were also assessed. RNA-seq was performed to investigate the mechanistic pathway changes. For in vitro studies, Sirt1 was overexpressed in BV2 microglial cells to compare with NAD+ treatment effects on mitochondrial injury and neuroinflammation. Results NAD+ administration rescued cognitive deficits and inhibited neuroinflammation by protecting mitochondria and decreasing ROS production in CCH rats. Results of mechanistic pathway analysis indicated that the detrimental effects of CCH might be associated with decreased gene expression of PPAR-γ co-activator1α (PGC-1α) and its upstream transcription factor Sirt1, while NAD+ treatment markedly reversed their decrease. In vitro study confirmed that NAD+ administration had protective effects on hypoxia-induced neuroinflammation and mitochondrial damage, as well as ROS production in BV2 microglia via Sirt1/PGC-1α pathway. Sirt1 overexpression mimicked the protective effects of NAD+ treatment in BV2 microglia. Conclusions NAD+ ameliorated cognitive impairment and dampened neuroinflammation in CCH models in vivo and in vitro, and these beneficial effects were associated with mitochondrial protection and ROS inhibition via activating Sirt1/PGC-1α pathway.

Cardioprotective effects of carvedilol on acute autoimmune myocarditis: anti-inflammatory effects associated with antioxidant property

2004 ◽  
Vol 286 (1) ◽  
pp. H83-H90 ◽  
Author(s):  
Zuyi Yuan ◽  
Keisuke Shioji ◽  
Yasuki Kihara ◽  
Hiroyuki Takenaka ◽  
Yoko Onozawa ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Experimental Models ◽  
Left Ventricular ◽  
Thiobarbituric Acid Reactive Substance ◽  
Autoimmune Myocarditis ◽  
Reactive Substance

Carvedilol, a new β-blocker with antioxidant properties, has been shown to be cardioprotective in experimental models of myocardial damage. We investigated whether carvedilol protects against experimental autoimmune myocarditis (EAM) because of its suppression of inflammatory cytokines and its antioxidant properties. We orally administered a vehicle, various doses of carvedilol, racemic carvedilol [ R(+)-carvedilol, an enantiomer of carvedilol without β-blocking activity], metoprolol, or propranolol to rats with EAM induced by porcine myosin for 3 wk. Echocardiographic study showed that the three β-blockers, except R(+)-carvedilol, suppressed left ventricular fractional shortening and decreased heart rates to the same extent. Carvedilol and R(+)-carvedilol, but not metoprolol or propranolol, markedly reduced the severity of myocarditis at the two different doses and suppressed thickening of the left ventricular posterior wall in rats with EAM. Only carvedilol suppressed myocardial mRNA expression of inflammatory cytokines and IL-1β protein expression in myocarditis. In addition, carvedilol and R(+)-carvedilol decreased myocardial protein carbonyl contents and myocardial thiobarbituric acid-reactive substance products in rats with EAM. The in vitro study showed that carvedilol and R(+)-carvedilol suppressed IL-1β production in LPS-stimulated U937 cells and that carvedilol and R(+)-carvedilol, but not metoprolol or propranolol, suppressed thiobarbituric acid-reactive substance products in myocardial membrane challenged by oxidative stress. It was also confirmed that probucol, an antioxidant, ameliorated EAM in vivo. Carvedilol protects against acute EAM in rats, and the superior cardioprotective effect of carvedilol compared with metoprolol and propranolol may be due to suppression of inflammatory cytokines associated with the antioxidant properties in addition to the hemodynamic modifications.

scholarly journals Hepatoprotective effects of partially purified fractions of Senna occidentalis ethanolic extract on diethyl nitrosamine-induced toxicity in Wistar rat

2021 ◽  
Vol 7 (8) ◽  
pp. 374
Author(s):  
Ojochenemi E. Yakubu ◽  
Eleojo B. Ojogbane ◽  
Francis O. Atanu ◽  
Chukwuka S. M. Udeh ◽  
Morayo E. Ale ◽  
...  
Keyword(s):  
Present Report ◽  
Ethanolic Extract ◽  
Thiobarbituric Acid ◽  
Wistar Rat ◽  
In Vivo Studies ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Group B

<p class="abstract"><strong>Background:</strong> Induction of toxicity using nitrosamines provides a reliable animal model for the study of oxidative damage to lipids, cellular membranes, proteins and DNA. In the present report, the effects of partially purified fractions of <em>Senna occidentalis</em> leaves on diethylnitrosamine intoxicated rats were studied.</p><p class="abstract"><strong>Methods:</strong> Fractions obtained from eluting the column with solvents of increasing polarity, n-hexane, chloroform, ethyl acetate, ethanol, methanol and distilled water were subjected to <em>in vitro</em> for their ability to scavenge 1, 1-dipheny l, 2-pycryl hydrazyl (DPPH) radical. Fraction 6a eluted with ethyl acetate:ethanol (50:50) possessed the highest antioxidant activity, this fraction was therefore selected for in vivo studies. Twenty rats, each weighing between 150 to 250 g were randomly allocated into four groups of five rats each. Hepatotoxicity was induced using a single intraperitoneal injection of diethylnitrosamine (DEN) at the 200 mg/kg body weight. Treatment was carried out for 3 weeks by oral gavage as follows: group A, normal control, group B, DEN control, group C, DEN+fraction (10 mg/kg), group D, DEN+silymarin (5 mg/kg).</p><p class="abstract"><strong>Results:</strong> The results showed that DEN toxicity significantly (p&lt;0.05) increased alanine transaminase (ALT) and aspartate transaminase (AST) activities and increased the level of thiobarbituric acid reactive substance (TBARS) in the liver. In contrast, the levels of bilirubin, total protein (TP) and albumin (ALB) decreased. However, treatment of rats with the extract significantly (p&lt;0.05) reduced the concentrations of TBARS, ALT, AST and bilirubin, but increased the concentration of TP and ALB.</p><p class="abstract"><strong>Conclusions:</strong> These results show hepatoprotective potentials of the fraction. Furthermore, GC-MS fingerprinting of fraction 6a revealed the presence of compounds with anticancer, antioxidant and anti-inflammatory properties confirming its high chance for exploration as a medicinal agent.</p>

scholarly journals Upregulation of SIRT1 and FOXO3a Contributes to The Protective Role of Estrogen on HPH in Rats

2020 ◽  
Author(s):  
Li Wang ◽  
Yadong Yuan ◽  
Xiaowei Gong ◽  
Jianjun Mao
Keyword(s):  
Pulmonary Artery ◽  
Protective Role ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Pulmonary Vascular Remodeling ◽  
Sprague Dawley Rats ◽  
Sirt1 Activator

Abstract Background: SIRT1 has anti-proliferation effects on cells through regulating the expression and activity of FOXOs. Estrogen (E2) has protective effects against hypoxic pulmonary hypertension (HPH), but the involvement of SIRT1 and FOXOs in the proliferation of pulmonary artery smooth muscle cells (PASMCs) and contribution to the effects of E2 on HPH are poorly understood. To use E2 to explore the roles of SIRT1 and FOXO3a in the pathogenesis and progression of HPH and pulmonary vascular remodeling (PVR) in vivo and in vitro.Methods: Female Sprague-Dawley rats with bilateral ovariectomy were randomized to normoxia, normoxia+E2, hypoxia, and hypoxia+E2. Serum E2 levels, hemodynamic, and pulmonary vascular pathomorphology were assessed. The anti-proliferation effect of E2 was determined in human PASMCs under hypoxia/normoxia. Immunohistochemistry, western blotting, and real-time PCR were used to assess SIRT1, FOXO3a, and PCNA in rat pulmonary artery and hPASMCs. SIRT1 activity was assayed.Results: Hypoxia increased mean pulmonary artery pressure (mPAP), medial width of pulmonary arterioles, right ventricular hypertrophy index (RVHI), decreased expression SIRT1 and FOXO3a and increased PCNA expression in rats; E2 alleviated these changes. In vitro, E2 significantly inhibited hypoxia-induced hPASMCs proliferation, associated with improvements in SIRT1 and FOXO3a expression, consistent with the in vivo results. SIRT1 inhibition attenuated the effects of E2 on hPASMCs proliferation and the expression of FOXO3a. A SIRT1 activator mimicked the effects of E2 on hPASMCs proliferation and the expression of FOXO3a.Conclusions: Upregulation of SIRT1 and FOXO3a contributes to the protective role of estrogen on HPH in rats, as supported by in vitro results using hPASMCs.

scholarly journals Effects of Plasma Treatment on the Bioactivity of Alkali-Treated Ceria-Stabilised Zirconia/Alumina Nanocomposite (NANOZR)

2020 ◽  
Vol 21 (20) ◽  
pp. 7476
Author(s):  
Seiji Takao ◽  
Satoshi Komasa ◽  
Akinori Agariguchi ◽  
Tetsuji Kusumoto ◽  
Giuseppe Pezzotti ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Plasma Treatment ◽  
Atmospheric Pressure Plasma ◽  
Material Surface ◽  
Sprague Dawley ◽  
Related Factors ◽  
Initial Adhesion ◽  
Marrow Mesenchymal Stem Cells

Zirconia ceramics such as ceria-stabilized zirconia/alumina nanocomposites (nano-ZR) are applied as implant materials due to their excellent mechanical properties. However, surface treatment is required to obtain sufficient biocompatibility. In the present study, we explored the material surface functionalization and assessed the initial adhesion of rat bone marrow mesenchymal stem cells, their osteogenic differentiation, and production of hard tissue, on plasma-treated alkali-modified nano-ZR. Superhydrophilicity was observed on the plasma-treated surface of alkali-treated nano-ZR along with hydroxide formation and reduced surface carbon. A decreased contact angle was also observed as nano-ZR attained an appropriate wettability index. Treated samples showed higher in vitro bovine serum albumin (BSA) adsorption, initial adhesion of bone marrow and endothelial vascular cells, high alkaline phosphatase activity, and increased expression of bone differentiation-related factors. Furthermore, the in vivo performance of treated nano-ZR was evaluated by implantation in the femur of male Sprague–Dawley rats. The results showed that the amount of bone formed after the plasma treatment of alkali-modified nano-ZR was higher than that of untreated nano-ZR. Thus, induction of superhydrophilicity in nano-ZR via atmospheric pressure plasma treatment affects bone marrow and vascular cell adhesion and promotes bone formation without altering other surface properties.

scholarly journals NAD+ Improves Cognitive Function and Reduces Neuroinflammation By Ameliorating Mitochondrial Damage and Decreasing ROS Production in Chronic Cerebral Hypoperfusion Models Through Sirt1/PGC-1α Pathway

2021 ◽  
Author(s):  
Yao Zhao ◽  
Jiawei Zhang ◽  
Yaling Zheng ◽  
Yaxuan Zhang ◽  
Xiaojie Zhang ◽  
...  
Keyword(s):  
Mitochondrial Damage ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Ros Production ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Mechanistic Pathway ◽  
Bv2 Microglia

Abstract Background: Microglial mediated neuroinflammation plays an important role in vascular dementia, and modulating neuroinflammation has emerged as a promising treatment target. NAD + shows anti-inflammatory and anti-oxidant effects in many neurodegenerative disease models, but its role in the chronic cerebral hypoperfusion (CCH) is still unclear. Methods: The bilateral common carotid artery occlusion (BCCAO) was performed to establish CCH models in Sprague-Dawley rats. The rats were given daily intraperitoneal injection of NAD + for 8 weeks. Behavioral test and markers for neuronal death and neuroinflammation were analyzed. Mitochondrial damage and ROS production in microglia were also assessed. RNA-seq was performed to investigate the mechanistic pathway changes. For in vitro studies, Sirt1 was overexpressed in BV2 microglial cells to compare with NAD + treatment effects on mitochondrial injury and neuroinflammation. Results: NAD + administration rescued cognitive deficits and inhibited neuroinflammation by protecting mitochondria and decreasing ROS production in CCH rats. Results of mechanistic pathway analysis indicated that the detrimental effects of CCH might be associated with decreased gene expression of PPAR-γ co-activator1α (PGC-1α) and its upstream transcription factor Sirt1 , while NAD + treatment markedly reversed their decrease. In vitro study confirmed that NAD + administration had protective effects on hypoxia induced neuroinflammation and mitochondrial damage, as well as ROS production in BV2 microglia via Sirt1/PGC-1α pathway. Sirt1 overexpression mimicked the protective effects of NAD + treatment in BV2 microglia.Conclusions: NAD + ameliorated cognitive impairment and dampened neuroinflammation in CCH models in vivo and vitro, and these beneficial effects were associated with mitochondrial protection and ROS inhibition via activating Sirt1/PGC-1α pathway. Keywords: Chronic cerebral hypoperfusion, microglia, NAD + , mitochondria, ROS

scholarly journals The Effects of Prunus spinosa L. Flower Extracts, Model Polyphenols and Phenolic Metabolites on Oxidative/Nitrative Modifications of Human Plasma Components with Particular Emphasis on Fibrinogen In Vitro

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 581
Author(s):  
Anna Marchelak ◽  
Joanna Kolodziejczyk-Czepas ◽  
Paulina Wasielewska ◽  
Pawel Nowak ◽  
Monika A. Olszewska
Keyword(s):  
Molecular Weight ◽  
Human Plasma ◽  
Structural Changes ◽  
Circulatory System ◽  
Thiobarbituric Acid ◽  
Protective Effects ◽  
Phenolic Metabolites ◽  
Prunus Spinosa

Oxidative post-translational modifications of fibrinogen (a multifunctional blood plasma protein essential for hemostasis) are associated with the pathogenesis of cardiovascular disorders (CVDs). Prunus spinosa flower is a herbal medicine used in an adjuvant treatment of CVDs and rich in polyphenolic antioxidants. In the present study, phytochemically standardized P. spinosa flower extracts, their primary native polyphenols and potential phenolic metabolites were evaluated in vitro for their protective effects on fibrinogen (isolated and in the human plasma matrix) using a panel of complementary methods (SDS-PAGE, western blot, C-ELISA, fluorometry, FRAP, TBARS). The results revealed that the tested analytes at in vivo relevant levels (1–5 µg/mL) considerably reduced the structural changes in the fibrinogen molecule under the oxidative stress conditions induced by peroxynitrite. In particular, they diminished the oxidation and/or nitration of amino acid residues, including tyrosine and tryptophan, as well as the formation of high molecular weight aggregates. The decrease in the levels of 3-nitrotyrosine was about 13.5–33.0% and 58.3–97.1% at 1 µg/mL and 50 µg/mL, respectively. The study indicated that low molecular weight polyphenols were crucial for the protective activity of the extracts toward fibrinogen and other human plasma components. The investigated model compounds effectively protected total plasma proteins and lipids against oxidative damage (by reducing the levels of 3-nitrotyrosine and thiobarbituric acid-reactive substances and normalizing/enhancing the non-enzymatic antioxidant capacity of plasma). The work provides insight into the role of native and metabolized polyphenols as contributory factors to the systemic activity of blackthorn flower extracts within the circulatory system.

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