Fresh Seed Supplementation of Syzygium Cumini Attenuated Oxidative Stress, Inflammation, Fibrosis, Iron Overload, Hepatic Dysfunction and Renal Injury in Acetaminophen Induced Rats

Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H2 can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H2 against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl’s stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H2 treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload.

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Pathophysiology of iron overload-induced renal injury and dysfunction: Roles of renal oxidative stress and systemic inflammatory mediators

Pathophysiology ◽

10.1016/j.pathophys.2019.03.002 ◽

2019 ◽

Vol 26 (2) ◽

pp. 175-180 ◽

Cited By ~ 2

Author(s):

A.O. Ige ◽

F.A. Ongele ◽

B.O. Adele ◽

I.E. Emediong ◽

A.O. Odetola ◽

...

Keyword(s):

Oxidative Stress ◽

Iron Overload ◽

Inflammatory Mediators ◽

Renal Injury

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Iron Metabolism in the Human Body and Setting its Hygienic Limits for Drinking Water. Review. Part 2

Hygiene and Sanitation ◽

10.33029/0016-9900-2020-99-5-504-508 ◽

2020 ◽

Vol 99 (5) ◽

pp. 504-508

Author(s):

Natalija A. Egorova ◽

N. V. Kanatnikova

Keyword(s):

Oxidative Stress ◽

Drinking Water ◽

Iron Overload ◽

Iron Metabolism ◽

Subcutaneous Tissue ◽

Allergic Diseases ◽

The Body ◽

Urogenital System ◽

High Iron Content ◽

Labile Iron Pool

Iron is an assential element for the growth, division, differentiation and functioning of any cell in the body. Iron is virtually important for human and danger at the same time, because with excessive accumulation it causes oxidative stress with formation of highly active oxygen radicals and reactive form of nitrogen that can destroy cell membranes, proteins, nucleic acids, reduce cell viability, with, according to modern concepts, can contribute to the development of many diseases (cardiovascular, rheumatic, gastrointestinal, neurodegenerative, oncological, metabolic and others), and also accelerate the aging process. Part 1 of this review discussed the issues of iron metabolism in human, including its regulation at the cellular and systemic levels, the intake, transport, use, accumulation and export of iron in cells, the role of the labile iron pool in the cytoplasm of cells and plasma non-transferrin bound iron. Data are provided on the causes, frequency and significance of iron overload in the formation of free radicals and the development of oxidative stress. Part 2 of the review provides information on diseases associated with iron overload as well as information on ferroptosis - a new type of iron-dependent regulated cell death. Attention is paid to the works of domestic authors, where it was found that prolonged use of drinking water with a high iron content is unfavorable for the population and leads to an increase in the overall incidence, the development of the diseases of the blood, skin and subcutaneous tissue, musculoskeletal system, digestive system, urogenital system, and allergic diseases. Separate publications are cited on the possibility of a negative effect of iron at concentrations in water of 0.3 mg/l and lower. The material of the review emphasizes the preventive significance of caution attitude to regulating iron in the water in the Russian Federation, where 1/3 of the population uses iron-containing water for drinking, and substantiate the feasibility of establishing a hygienic limit for iron in water not higher than 0.3 mg/l.

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Kahweol Ameliorates Cisplatin-Induced Acute Kidney Injury through Pleiotropic Effects in Mice

Biomedicines ◽

10.3390/biomedicines8120572 ◽

2020 ◽

Vol 8 (12) ◽

pp. 572

Author(s):

Jung-Yeon Kim ◽

Jungmin Jo ◽

Jaechan Leem ◽

Kwan-Kyu Park

Keyword(s):

Oxidative Stress ◽

Acute Kidney Injury ◽

Renal Injury ◽

Manganese Superoxide Dismutase ◽

Immune Cell ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Kidney Injury ◽

Pleiotropic Effects ◽

Induced Apoptosis ◽

Vascular Adhesion

Cisplatin is an effective chemotherapeutic agent, but its clinical use is frequently limited by its nephrotoxicity. The pathogenesis of cisplatin-induced acute kidney injury (AKI) remains incompletely understood, but oxidative stress, tubular cell death, and inflammation are considered important contributors to cisplatin-induced renal injury. Kahweol is a natural diterpene extracted from coffee beans and has been shown to possess anti-oxidative and anti-inflammatory properties. However, its role in cisplatin-induced nephrotoxicity remains undetermined. Therefore, we investigated whether kahweol exerts a protective effect against cisplatin-induced renal injury. Additionally, its mechanisms were also examined. Administration of kahweol attenuated renal dysfunction and histopathological damage together with inhibition of oxidative stress in cisplatin-injected mice. Increased expression of nicotinamide adenine dinucleotide phosphate oxidase 4 and decreased expression of manganese superoxide dismutase and catalase after cisplatin treatment were significantly reversed by kahweol. Moreover, kahweol inhibited cisplatin-induced apoptosis and necroptosis in the kidneys. Finally, kahweol reduced inflammatory cytokine production and immune cell accumulation together with suppression of nuclear factor kappa-B pathway and downregulation of vascular adhesion molecules. Together, these results suggest that kahweol ameliorates cisplatin-induced renal injury via its pleiotropic effects and might be a potential preventive option against cisplatin-induced nephrotoxicity.

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Gene expression reveals vulnerability to oxidative stress and interstitial fibrosis of renal outer medulla to nonhypertensive elevations of ANG II

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00257.2002 ◽

2003 ◽

Vol 284 (5) ◽

pp. R1219-R1230 ◽

Cited By ~ 20

Author(s):

Baozhi Yuan ◽

Mingyu Liang ◽

Zhizhang Yang ◽

Elizabeth Rute ◽

Norman Taylor ◽

...

Keyword(s):

Oxidative Stress ◽

Western Blot ◽

Renal Injury ◽

Interstitial Fibrosis ◽

Control Period ◽

Renal Medulla ◽

Differentially Expressed ◽

Ang Ii ◽

Outer Medulla ◽

Renal Outer Medulla

The present study was designed to determine whether nonhypertensive elevations of plasma ANG II would modify the expression of genes involved in renal injury that could influence oxidative stress and extracellular matrix formation in the renal medulla using microarray, Northern, and Western blot techniques. Sprague-Dawley rats were infused intravenously with either ANG II (5 ng · kg−1 · min−1) or vehicle for 7 days ( n = 6/group). Mean arterial pressure averaged 110 ± 0.6 mmHg during the control period and 113 ± 0.4 mmHg after ANG II. The mRNA of 1,751 genes (∼80% of all currently known rat genes) that was differentially expressed (ANG II vs. saline) in renal outer and inner medulla was determined. The results of 12 hybridizations indicated that in response to ANG II, 11 genes were upregulated and 25 were downregulated in the outer medulla, while 11 were upregulated and 13 were downregulated in the inner medulla. These differentially expressed genes, most of which were not known previously to be affected by ANG II in the renal medulla, were found to group into eight physiological pathways known to influence renal injury and kidney function. Particularly, expression of several genes would be expected to increase oxidative stress and interstitial fibrosis in the outer medulla. Western blot analyses confirmed increased expression of transforming growth factor-β1 and collagen type IV proteins in the outer medulla. Results demonstrate that nonhypertensive elevations of plasma ANG II can significantly alter the expression of a variety of genes in the renal outer medulla and suggested the vulnerability of the renal outer medulla to the injurious effect of ANG II.

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Salvianolic Acid B Prevents Iodinated Contrast Media-Induced Acute Renal Injury in Rats via the PI3K/Akt/Nrf2 Pathway

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/7079487 ◽

2016 ◽

Vol 2016 ◽

pp. 1-11 ◽

Cited By ~ 26

Author(s):

Liu Tongqiang ◽

Liu Shaopeng ◽

Yu Xiaofang ◽

Song Nana ◽

Xu Xialian ◽

...

Keyword(s):

Oxidative Stress ◽

Contrast Media ◽

Renal Injury ◽

Salvianolic Acid B ◽

Pi3k Inhibitor ◽

Iodinated Contrast Media ◽

Acute Renal Injury ◽

Nrf2 Pathway ◽

Salvianolic Acid ◽

Iodinated Contrast

Contrast-induced acute renal injury (CI-AKI) has become a common cause of hospital-acquired renal failure. However, the development of prophylaxis strategies and approved therapies for CI-AKI is limited. Salvianolic acid B (SB) can treat cardiovascular-related diseases. The aim of the present study was to assess the effect of SB on prevention of CI-AKI and explore its underlying mechanisms. We examined its effectiveness of preventing renal injury in a novel CI-AKI rat model. Compared with saline, intravenous SB pretreatment significantly attenuated elevations in serum creatinine and the histological changes of renal tubular injuries, reduced the number of apoptosis-positive tubular cells, activated Nrf2, and lowered the levels of renal oxidative stress induced by iodinated contrast media. The above renoprotection of SB was abolished by the PI3K inhibitor (wortmannin). In HK-2 cells, SB activated Nrf2 and decreased the levels of oxidative stress induced by hydrogen peroxide and subsequently improved cell viability. The above cytoprotection of SB was blocked by the PI3K inhibitor (wortmannin) or siNrf2. Thus, our results demonstrate that, due to its antioxidant properties, SB has the potential to effectively prevent CI-AKI via the PI3K/Akt/Nrf2 pathway.

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