Coenzyme Q10 supplementation affects cellular ionic balance: relevance to aging.

Aging results into disruptive physiological functioning and cellular processes that affect the composition and structure of the plasma membrane. The plasma membrane is the major regulator of ionic homeostasis that regulates the functioning of membrane transporters and exchangers. Coenzyme Q10 is a lipid-soluble antioxidant molecule that declines during aging and age-associated diseases. The present study aims to explore the role of Coenzyme Q10 supplementation to rats during aging on membrane transporters and redox biomarkers. The study was conducted on young and old male Wistar rats supplemented with 20 mg/kg b.w. of Coenzyme Q10 per day. After a period of 28 days, rats were sacrificed and erythrocyte membrane was isolated. The result exhibits significant decline in biomarkers of oxidative stress in old control rats when compared with young control. The effect of Coenzyme Q10 supplementation was more pronounced in old rats. The functioning of membrane transporters and Na+/H+ exchanger showed potential return to normal levels in the Coenzyme Q10 treated rats. Overall, the results demonstrate that Coenzyme Q10 plays an important role in maintaining redox balance in cells which interconnects with membrane integrity. Thus, Coenzyme Q10 supplementation may play an important role in protecting age related alterations in erythrocyte membrane physiology.

Berberine attenuates brain aging via stabilizing redox homeostasis and inflammation in an accelerated senescence model of Wistar rats.

Aging is a multifaceted and progressive physiological change of the organism categorized by the accumulation of deteriorating processes, which ultimately compromise the biological functions. The objective of this study was to investigate the anti-aging potential of berberine (BBR) in D-galactose (D-Gal) induced aging in rat models. In this study, male Wistar rats were divided into four groups: The control group was given only vehicle, the BBR group was treated with berberine orally, the D-Gal group was treated with D-galactose subcutaneously and the BBR + D-Gal group was treated with D-galactose and berberine simultaneously. D-galactose exposure elevated the pro-oxidants such as malondialdehyde (MDA) level, protein carbonyl and advanced oxidation protein products (AOPP) in the brain. It decreased the anti-oxidants such as reduced glutathione (GSH) and ferric reducing antioxidant potential (FRAP) in the brain. D-galactose treatment also reduced the mitochondrial complexes (I, II, III and IV) activities and elevated the inflammatory markers such as interleukine-6 (IL-6), tumor necrosis factor- α (TNF-α) and C-reactive protein (CRP). The mRNA expressions of IL-6 and TNF-α in the brain were upregulated following D-galactose exposure. Berberine co-treatment in D-galactose induced aging rat model prevented the alteration of pro-oxidant and anti-oxidant in the brain. Berberine treatment restored the mitochondrial complex activities in the brain and also normalized the inflammatory markers. Based on these findings we conclude that berberine treatment has the potential to mitigate brain aging in rats via stabilizing the redox equilibrium and neuroinflammation.

Curcumin displays a potent caloric restriction mimetic effect in an accelerated senescent model of rat.

Curcumin, a strong natural compound with numerous health benefits, is extracted from the Curcuma longa. According to recent research findings, it also acts as a calorie restriction mimetic. We examined established aging biomarkers in erythrocytes and plasma and tested a persistent oral dietary dose of curcumin in young and D-galactose-induced accelerated rat aging models. For four weeks, D-gal (300 mg/kg b.w. subcutaneously) and curcumin (200 mg/kg b.w. oral) were administered simultaneously to test the protective effects of curcumin against D-galactose-induced accelerated aging and oxidative stress. In the accelerated senescent rat model, we discovered a significant rise in protein carbonyl, malonaldehyde (MDA), and advanced oxidation protein products. Increased levels of catalase, superoxide dismutase, ferric-reducing antioxidant potential, and reduced glutathione (GSH) were observed. Our findings reveal that curcumin has characteristics resembling a calorie restriction mimic and can successfully maintain redox equilibrium throughout the aging process in rat erythrocytes and plasma.

Acarbose Mitigates Age-Dependent Alterations in Erythrocyte Membrane Transporters During Aging in Rats.

Acarbose (ACA), a well-studied and effective inhibitor of α-amylase and α-glucosidase, is a postprandial-acting antidiabetic medicine. The membrane of the erythrocyte is an excellent tool for analyzing different physiological and biochemical activities since it experiences a range of metabolic alterations throughout aging. It is uncertain if ACA modulates erythrocyte membrane activities in an age-dependent manner. As a result, the current study was conducted to explore the influence of ACA on age-dependent deteriorated functions of transporters/exchangers, disrupted levels of various biomarkers such as lipid hydroperoxides (LHs), protein carbonyl (PCO), sialic acid (SA), total thiol (-SH), and erythrocyte membrane osmotic fragility. In addition to a concurrent increase in Na+/H+ exchanger activity and concentration of LH, PCO, and osmotic fragility, we also detected a considerable decrease in membrane-linked activities of Ca2+-ATPase (PMCA) and Na+/K+-ATPase (NKA), as well as concentrations of SA and -SH in old-aged rats. The aging-induced impairment of the activities of membrane-bound ATPases and the changed levels of redox biomarkers were shown to be effectively restored by ACA treatment.

Berberine may provide redox homeostasis during aging in rats.

Aging is a natural phenomenon, which is characterised by progressive physiological changes at cellular and organ level. During aging, the defence mechanism of an organism declines over the period of time. The aim of this study was to investigate the biological efficacy of berberine in D-galactose induced aging rat models. For the study, rats were divided into four groups: Control received only vehicle, BBR received berberine orally, D-Gal received D-galactose subcutaneously and BBR + D-Gal received D-galactose and berberine simultaneously. D-galactose treatment increased the pro-oxidants such as malondialdehyde (MDA) level, protein carbonyl, plasma membrane redox system (PMRS) and advanced oxidation protein products (AOPP) in the erythrocytes or plasma. It reduced the anti-oxidant level such as reduced glutathione (GSH), ferric reducing ability of plasma (FRAP), plasma thiols, sialic acid and membrane transporters like Na+/K+ ATPase and Ca2+ ATPase activity in the erythrocyte membrane. Co-treatment of berberine in D-galactose induced aging rat models restored pro-oxidants and anti-oxidants in erythrocytes. Berberine also restored the activity of Na+/K+ ATPase and Ca2+ ATPase in the erythrocyte membrane. On the basis of these findings, we suggest that berberine treatment could attenuate erythrocyte aging in rats through stabilisation of the redox equilibrium.

Acarbose, an α-Glucosidase Inhibitor, Maintains Altered Redox Homeostasis During Aging by Targeting Glucose Metabolism in Rat Erythrocytes.

Increasing age is the single largest risk factor for a variety of chronic illnesses. As a result, improving the capability to target the aging process leads to an increased health span. A lack of appropriate glucoregulatory control is a recurring issue associated with aging and chronic illness, even though many longevity therapies result in the preservation of glucoregulatory control. In this study, we suggest that targeting glucose metabolism to improve regulatory control can help slow the aging process. Male Wistar rats, both young (age 4 months) and old (age 24 months), were given acarbose (ACA) (30 mg/kg b.w.) for 6 weeks. An array of oxidative stress indicators was assessed after the treatment period, including plasma antioxidant capacity as determined by the ferric reducing ability of plasma (FRAP), reactive oxygen species (ROS), lipid peroxidation (malondialdehyde [MDA]), reduced glutathione (GSH), total plasma thiol (sulfhydryl [SH]), plasma membrane redox system (PMRS), protein carbonyl (PCO), advanced oxidation protein products (AOPPs), advanced glycation end products (AGEs), and sialic acid (SA) in control and treated groups. When compared with controls, ACA administration increased FRAP, GSH, SH, and PMRS activities in both age groups. The treated groups, on the contrary, showed substantial decreases in ROS, MDA, PCO, AOPP, AGE, and SA levels. The effect of ACA on almost all parameters was more evident in old-age rats. ACA significantly increased PMRS activity in young rats; here the effect was less prominent in old rats. Our data support the restoration of antioxidant levels in older rats after short-term ACA treatment. The findings corroborate the potential role of ACA as a putative calorie restriction mimetic.

Modulatory effect of exogenous Coenzyme Q10 on redox and inflammatory biomarkers during aging in rats.

An impaired redox homeostasis is an important hallmark of biological aging. Coenzyme Q10 is an endogenous lipophilic antioxidant that decreases with age and has been linked to oxidative stress. The purpose of this study was to evaluate the effect of CoQ10 supplementation on redox homeostasis and levels of inflammatory cytokines in young and old rats. Male Wistar rats (young and old) were randomly divided into four groups (n = 6). Group I: young control, Group II: young rats treated with CoQ10, Group III: old control, Group IV: old rats treated with CoQ10. CoQ10 (20 mg/kg) was administered daily to Group II and IV via oral gavage. After 28 days of treatment, rats were sacrificed and biomarkers of oxidative stress and inflammatory cytokines were evaluated. Results demonstrated a significant (p ≤ 0.05) increase in malondialdehyde, protein carbonyl oxidation, advanced oxidation protein products, inflammatory cytokines: CRP, IL-6, TNF-α, and a decline in levels of superoxide dismutase, catalase, reduced glutathione, ferric reducing antioxidant potential in plasma and plasma membrane redox system in old rats when compared to young rats. After treatment with CoQ10 significant decrease in the level of MDA, PCO, AOPP, CRP, IL-6, and TNF-α was observed. Also, significant up-regulation of SOD, CAT, GSH, FRAP, and PMRS was observed. The results show that supplementing rats with CoQ10 aids in the maintenance of redox equilibrium with replenishment of antioxidant reserves and down-regulation of inflammatory biomarkers. Thus CoQ10 supplementation could be a potential anti-aging therapy.

Melatonin stabilizes age-dependent alterations in erythrocyte membrane induced by 'Artificial Light at Night' in a chronodisrupted model of rat.

Growing evidence has shown that Artificial light at night (ALAN) is one of the threatening risk factors which disrupt circadian homeodynamics of cellular processes. The chronobiological role of melatonin seems to represent an important aspect of its contribution to healthy aging. In the present study, we examined the age dependent effect of melatonin on erythrocyte membrane transporters and oxidative stress biomarkers against ALAN to understand the degree of photo-oxidative damage in chronodisrupted rat model. Young (3 months) and old (24 months) male Wistar rats were subdivided in the following four young groups (n = 4) ; (i) control (ii) melatonin (10 mg/kg) (iii) ALAN (500 lx) (iv) ALAN (500 lx) + melatonin (10 mg/kg) and four old groups (n = 4); (v) control (vi) melatonin (10 mg/kg) (vii) ALAN (500 lx) (viii) ALAN (500 lx) + melatonin (10 mg/kg) to the experimental conditions for 10 days. Our findings demonstrated that ALAN significantly enhanced erythrocyte membrane lipid hydroperoxides (LHPs), protein carbonyl (PCO) while reduced total thiol (T-SH), and sialic acid (SA) level with higher amplitude in old ALAN group is restored by exogenous supplementation of melatonin. Activity of membrane transporters, sodium potassium ATPase (NKA) and plasma membrane calcium ion ATPase (PMCA) is significantly reduced meanwhile sodium hydrogen exchanger (NHE) activity is enhanced under the influence of ALAN with higher extent in old groups is effectively ameliorated by melatonin treatment. Further melatonin reduced osmotic fragility of erythrocyte in both young and old rats. It has been concluded from results that ALAN provoked redox insult and disrupt transporters activity more prominently in erythrocyte membrane of aged groups. Exogenous supplementation of melatonin is one of the possible therapeutic approaches to reinforce circadian modulations against ALAN in aged populations.