Dietary modulation of prostanoid synthesis in the aging process: role of cyclooxygenase-2

Chung, Habong; Kim, Hyon-Jeen; Shim, Kyung-Hee; Kim, Kyu‐Won

doi:10.1016/s0047-6374(99)00061-5

Cited by 37 publications

(20 citation statements)

References 42 publications

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“…Protein overload of proximal tubule cells is also harmful since it activates intracellular signals that induce an increase in vasoactive, inflammatory mediators and growth factors (1,15). The activation of COX2 during HPI in the hypertensive males could contribute to kidney disease progression and end-stage renal failure since it may be accompanied by an elevation in reactive oxidant species production, which exacerbates proinflammatory PG action (5). Sex hormones may also be involved in the different evolution of renal function between males and females in response to the prolonged HPI.…”

Section: Discussionmentioning

confidence: 99%

Renal effects of prolonged high protein intake and COX2 inhibition on hypertensive rats with altered renal development

Reverte

Tapia²,

Moreno³

et al. 2011

American Journal of Physiology-Renal Physiology

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Reverte V, Tapia A, Moreno JM, Rodríguez L, Salazar F, Llinás MT, Salazar FJ. Renal effects of prolonged high protein intake and COX2 inhibition on hypertensive rats with altered renal development. Am J Physiol Renal Physiol 301: F327-F333, 2011. First published May 25, 2011 doi:10.1152/ajprenal.00110.2011.-Cyclooxygenase 2 (COX2) is involved in regulating renal hemodynamics after renal ablation. It is also known that high protein intake (HPI) leads to a deterioration of renal function when there is preexisting renal disease and that there are important gender differences in the regulation of renal function. This study tested the hypothesis that the role of COX2 in regulating renal function and the renal hemodynamic effects elicited by HPI are enhanced when nephrogenesis is altered during renal development. It was also expected that the role of COX2 and the effects elicited by HPI are age and sex dependent. Newborn Sprague-Dawley rats were treated with an AT1 ANG II receptor antagonist during the nephrogenic period (ARAnp). Experiments were performed at 3-4 and 10 -11 mo of age. Arterial pressure was elevated (P Ͻ 0.05) at both ages and in both sexes of ARAnptreated rats. Renal COX2 expression was only elevated (P Ͻ 0.05) at 10 -11 mo of age in both sexes of ARAnp-treated rats. COX2 inhibition induced greater renal vasoconstriction in male and female hypertensive than in normotensive rats at both ages. HPI did not induce glomerular filtration rate (GFR) in the youngest hypertensive rats and in the oldest female hypertensive rats. However, the GFR decreased during HPI (0.63 Ϯ 0.07 to 0.19 Ϯ 0.05 ml/min) in the oldest male hypertensive rats. The HPI-induced increment in proteinuria was greater (P Ͻ 0.05) in male (99 Ϯ 22 mg/day) than in female (30 Ϯ 8 mg/day) hypertensive rats. These results show that COX2 plays an important role in the regulation of renal function when renal development is altered and that prolonged HPI can lead to a renal insufficiency in males but not in females with reduced nephron endowment.hypertension; proteinuria; renal function SEVERAL STUDIES HAVE PROPOSED that an alteration in nephrogenesis leads to a compensatory glomerular hypertrophy and an accelerated deterioration of renal function that are sex dependent (2,8,21,31). It has been reported that the compensatory glomerular changes that occur in male animals after subtotal ablation of renal mass are mediated by an increase in cyclooxygenase 2 (COX2) activity (7,27). However, it is unknown to what extent COX2 is involved in the regulation of renal function when nephron endowment decreases during renal development and whether this importance of COX2 is greater in males than in females. One hypothesis tested in this study is that COX2-derived metabolites are involved in the regulation of renal function when nephrogenesis is altered during the late nephrogenic period and that the role of COX2 is sex and aging dependent. A sex-dependent difference was expected since it has been reported in other mechanisms involved in the regulation of ren...

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Section: Discussionmentioning

confidence: 99%

Renal effects of prolonged high protein intake and COX2 inhibition on hypertensive rats with altered renal development

Reverte

Tapia²,

Moreno³

et al. 2011

American Journal of Physiology-Renal Physiology

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“…iNOS and COX-2 proteins are known to be involved in the pathogenesis of many chronic diseases associated with oxidative stress. 41,42) These proteins have a close relationship in the activation of NF-kB, which translocates to the nucleus where it regulates iNOS and COX-2. 35,43) Therefore, iNOS and COX-2 proteins are good indicators of cellular oxidation.…”

Section: Discussionmentioning

confidence: 99%

Anti-aging Effects of Cyanidin under a Stress-Induced Premature Senescence Cellular System

Choi

Kim

Park

et al. 2010

Biological & Pharmaceutical Bulletin

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Reactive oxygen species (ROS) including superoxide (O 2 Ϫ ), hydrogen peroxide (H 2 O 2 ), and hydroxyl radical ( · OH) are over-produced under pathological conditions and during the aging process. ROS can cause DNA strand breaks, base modifications, lipid peroxidation, and protein modifications, resulting in oxidative stress. Emerging evidence indicates that ROS are important risk factors in functional disorders or tissue injury related to the aging process. [1][2][3][4] According to the free radical theory of aging, the aging process is thought to lead to an imbalance between oxidative damage and antioxidative defense.5-9) Therefore, it has been suggested that the prevention of oxidative damage through the enhancement of antioxidative defense status may counteract aging and age-associated disorders such as cancer, 10) cardiovascular disorders, 11) and some neurodegenerative disorders.12) To delay the aging process through the attenuation of oxidative stress induced by excessive ROS, agents with antiaging effects have attracted much attention. In particular, anthocyanins are well known as antioxidants.13) Although the antioxidative effects of cyanidin, the most prevalent anthocyanin in the plant kingdom, [14][15][16] have been reported, its effects on aging and lifespan have not yet been studied.Although there are several experimental models for studying aging, human diploid fibroblasts (HDFs) have become a classic experimental model of cellular aging and are used to study aging-associated molecular changes in human cells. After serial passage, HDFs lose the ability to proliferate and become senescent, showing cellular changes related to the aging process, 17,18) termed replicative senescence (RS). In addition, HDFs exhibit the stress-induced premature senescence (SIPS) phenotype after being subjected to different sub-lethal stressors, including oxidative stress, 19,20) and this SIPS phenotype is almost identical to the phenotype associated with RS.20) The present study focused on the anti-aging activity of cyanidin and its related protective mechanisms against aging under SIPS using WI-38 human fibroblast cells. Furthermore, the effect of cyanidin on lifespan was also investigated. MATERIALS AND METHODSReagents Basal medium eagle (BME), paraformaldehyde, and Triton X-100 were purchased from Sigma Chemical Co. , and Nakalai (Kyoto, Japan), respectively. Monoclonal anti-cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), goat monoclonal anti-mouse immunoglobulin (IgG), and goat anti-rabbit IgG horseradish peroxidase-conjugated secondary antibodies were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, U.S.A.).Cell Culture and Treatment The WI-38 cells (human embryonic lung-derived diploid fibroblasts) were originally obtained from the ATCC (American Type Culture Collection, U.S.A.). WI-38 HDFs at population doubling levels (PDLs) of 26.0 were seeded at a density of 10 5 cells/ml in 6-or 96-well culture plates and incubated for 2 h. Three-hundred micromolars of H 2 O 2 was treated for 60 min ...

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“…The relative contribution of COX-derived ROS to the total ROS markedly increased in aged rat kidney: 13.92% in the 6-month-old rat and 26.36% in the 24-month-old rat . The production of PG (PGE 2 TXA 2 , and PGI 2 ), COX-2 mRNA, and protein levels were also found to increase correspondingly with age-related oxidative stress (Chung et al, 1999a;Kim et al, 2000).…”

Section: Effects Of Prostaglandins and Cyclooxygenase-2mentioning

confidence: 99%

“…We investigated CR's anti-inflammatory action in conjugation with COX-derived ROS generation utilizing indomethacin (Chung et al, 1999a;Kim et al, 2000). Data showed that CR suppresses COX-derived ROS generation from 26.36% in AL to 16.55% in CR group, and concomitantly blunted the COX activity and the production of TXA 2 , PGI 2 , and PGE 2 .…”

Section: Modulation Of Molecular Inflammation By Caloriementioning

confidence: 99%

Molecular inflammation hypothesis of aging based on the anti‐aging mechanism of calorie restriction

Chung

Kim

et al. 2002

Microscopy Res & Technique

273

186

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Accumulating evidence strongly suggests that oxidative stress underlies aging processes. Research provides consistent evidence that calorie restriction (CR) reduces age-related oxidative stress and has anti-inflammatory properties. However, information is lacking on the molecular mechanism that would better define the interrelation of reactive oxygen species and nitrogen species and the pro-inflammatory states of the aging process. In this review, the biochemical and molecular bases of the inflammatory process in the aging process are analyzed to delineate the molecular inflammation hypothesis of aging. The key players involved in the proposed hypothesis are the age-related upregulation of NF-kappa B, IL-1 beta, IL-6, TNFalpha, cyclooxygenase-2, and inducible NO synthase, all of which are attenuated by CR. Furthermore, age-related NF kappa B activation is associated with phosphorylation by I kappa B kinase/NIK and MAPKs, while CR blocked these activation processes. The modulation of these factors provides molecular insights of the anti-inflammatory action of CR in relation to the aging process. Based on available finding and our recent supporting evidence, we prefer to use "molecular inflammation" to emphasize the importance of the molecular reaction mechanisms and their aberrance, predisposing to fully expressed chronic inflammatory phenomena. It was further proposed that CR's major force of the regulation of redox-sensitive inflammation may well be its life-prolonging action.

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Dietary modulation of prostanoid synthesis in the aging process: role of cyclooxygenase-2

Cited by 37 publications

References 42 publications

Renal effects of prolonged high protein intake and COX2 inhibition on hypertensive rats with altered renal development

Renal effects of prolonged high protein intake and COX2 inhibition on hypertensive rats with altered renal development

Anti-aging Effects of Cyanidin under a Stress-Induced Premature Senescence Cellular System

Molecular inflammation hypothesis of aging based on the anti‐aging mechanism of calorie restriction

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