Protective effects of curcumin against ischemia-reperfusion injury in the liver

Bavarsad, Kowsar; Riahi, Maryam Matbou; Saadat, Saeideh; Barreto, George E.; Atkin, Stephen L.; Sahebkar, Amirhossein

doi:10.1016/j.phrs.2018.12.014

Cited by 58 publications

(38 citation statements)

References 125 publications

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“…Curcumin dietary supplementation tended to decrease the serum concentration of GGT. This enzyme increases their activity in the case of liver injury or overload (Bavarsada et al 2019). Previous researchers have stated that curcumin has a hepatoprotective action (Khan et al 2019) that possibly explains this reduction in liver enzyme.…”

Section: Discussionmentioning

confidence: 98%

Effect of curcumin dietary supplementation on growth performance, physiology, carcass characteristics and meat quality in lambs

Marcon

Souza

Baldissera

et al. 2021

Annals of Animal Science

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This study evaluated the effects of curcumin dietary supplementation on growth, physiology, carcass characteristics and meat quality in lambs. Thirty-two male Lacaune lambs (15.6 ± 0.63 kg, 60 ± 2.8 days of age) were randomly allocated in 16 pens (four treatments of four replicates with two lambs each) for 30 days. The animals were assigned to the following treatments: T0, T100, T200 and T300, representing 0, 100, 200 and 300 mg of curcumin/kg of concentrate, respectively. Curcumin dietary supplementation increased (P = 0.02) weight gain; on regression analysis, 315.1 mg curcumin/kg of concentrate was the dosage that provided the greatest weight gain. T200 and T300 lambs had lower (P = 0.04) erythrocytes numbers; T100 and T300 lambs had lower (P = 0.01) leukocyte numbers and T300 lambs had lower (P = 0.04) lymphocyte numbers, compared to T0 lambs. Globulin levels were significantly greater in the T200 group (P = 0.04) only on day 15 but not day 30; levels of total protein were significantly higher (P = 0.01) only in T200 and T300 group on day 15 and only in T200 group on d 30. Gamma-glutamyltransferase concentrations tended to be lower (P = 0.08) in T100, T200 and T300 group on d 15, and only in the T100 group on d 30. Curcumin dietary supplementation increased (P = 0.01) the serum activity of antioxidant enzymes and reduced (P = 0.01) levels of reactive oxygen species. In meat samples, T200 and T300 had greater total antioxidant capacity (P = 0.03) and lower (P = 0.01) lipoperoxidation rates. In carcasses, T300 lambs had greater (P ≤ 0.02) cooling weight losses and yields than did T0 lambs. Curcumin dietary supplementation also reduced (P ≤ 0.03) redness and yellowness. T200 and T300 lambs had fewer (P = 0.01) cooking losses and T200 lambs had greater (P = 0.03) water holding capacity than did T0 lambs. These findings suggest that curcumin dietary supplementation improves growth and antioxidant responses, as well as influencing meat quality in lambs.

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Section: Discussionmentioning

confidence: 98%

Effect of curcumin dietary supplementation on growth performance, physiology, carcass characteristics and meat quality in lambs

Marcon

Souza

Baldissera

et al. 2021

Annals of Animal Science

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“…Tissue injuries, including those to liver [ 78 ], brain [ 79 ], heart [ 80 ], and intestine [ 81 ], are related to excessive/aberrant inflammation, oxidative stress, mitochondrial dysfunction, and apoptosis [ 82 ]. Mitochondria are known as the energy factory of cells [ 83 ], and inflammation, ROS generation, mitochondrial dysfunction, and apoptosis are also found in I/R injuries [ 84 ].…”

Section: Discussionmentioning

confidence: 99%

Cinnamaldehyde protects against rat intestinal ischemia/reperfusion injuries by synergistic inhibition of NF-κB and p53

Almoiliqy

Wen

et al. 2020

Acta Pharmacol Sin

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Our preliminary study shows that cinnamaldehyde (CA) could protect against intestinal ischemia/reperfusion (I/R) injuries, in which p53 and NF-κB p65 play a synergistic role. In this study, we conducted in vivo and in vitro experiments to verify this proposal. SD rats were pretreated with CA (10 or 40 mg · kg −1 · d −1 , ig) for 3 days, then subjected to 1 h mesenteric ischemia followed by 2 h reperfusion. CA pretreatment dose-dependently ameliorated morphological damage and reduced inflammation evidenced by decreased TNF-α, IL-1β, and IL-6 levels and MPO activity in I/R-treated intestinal tissues. CA pretreatment also attenuated oxidative stress through restoring SOD, GSH, LDH, and MDA levels in I/R-treated intestinal tissues. Furthermore, CA pretreatment significantly reduced the expression of inflammation/apoptosis-related NF-κB p65, IKKβ, IK-α, and NF-κB p50, and downregulated apoptotic protein expression including p53, Bax, caspase-9 and caspase-3, and restoring Bcl-2, in I/R-treated intestinal tissues. We pretreated IEC-6 cells in vitro with CA for 24 h, followed by 4 h hypoxia and 3 h reoxygenation (H/R) incubation. Pretreatment with CA (3.125, 6.25, and 12.5 μmol · L −1 ) significantly reversed H/R-induced reduction of IEC-6 cell viability. CA pretreatment significantly suppressed oxidative stress, NF-κB activation and apoptosis in H/R-treated IEC-6 cells. Moreover, CA pretreatment significantly reversed mitochondrial dysfunction in H/R-treated IEC-6 cells. CA pretreatment inhibited the nuclear translocation of p53 and NF-κB p65 in H/R-treated IEC-6 cells. Double knockdown or overexpression of p53 and NF-κB p65 caused a synergistic reduction or elevation of p53 compared with knockdown or overexpression of p53 or NF-κB p65 alone. In H/R-treated IEC-6 cells with double knockdown or overexpression of NF-κB p65 and p53, CA pretreatment caused neither further decrease nor increase of NF-κB p65 or p53 expression, suggesting that CA-induced synergistic inhibition on both NF-κB and p53 played a key role in ameliorating intestinal I/R injuries. Finally, we used immunoprecipitation assay to demonstrate an interaction between p53 and NF-κB p65, showing the basis for CA-induced synergistic inhibition. Our results provide valuable information for further studies.

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“…Such pharmacological success relies on the phytochemical abilities of acting on many critical pathways, showing anti-inflammatory (Tham et al, 2010), anti-oxidant (Alexandrow et al, 2012), anti-microbial (Moghadamtousi et al, 2014), and anti-apoptotic (Yu et al, 2010; Jaisin et al, 2011) effects, as well as capability to promote stem cell differentiation (Gu et al, 2012; Mujoo et al, 2012; Chen et al, 2014). Effects of curcumin on mitochondrial function have also been reported (Bavarsad et al, 2018; He et al, 2018; Hsiao et al, 2018; Momekova et al, 2018; Naserzadeh et al, 2018) and furthermore, hormetic effects of curcumin are receiving increased attention (Moghaddam et al, 2018). Curcumin pleiotropic activity is due to its chemical structure, and specifically to the o-methoxy phenolic groups (Priyadarsini and Indira, 2014), which are central for chemical reactions.…”

Section: Introductionmentioning

confidence: 99%

Curcumin: Novel Treatment in Neonatal Hypoxic-Ischemic Brain Injury

Rocha‐Ferreira

Sisa²,

Bright³

et al. 2019

Front. Physiol.

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Hypoxic-ischemic encephalopathy (HIE) is a major cause of mortality and morbidity in neonates, with an estimated global incidence of 3/1,000 live births. HIE brain damage is associated with an inflammatory response and oxidative stress, resulting in the activation of cell death pathways. At present, therapeutic hypothermia is the only clinically approved treatment available for HIE. This approach, however, is only partially effective. Therefore, there is an unmet clinical need for the development of novel therapeutic interventions for the treatment of HIE. Curcumin is an antioxidant reactive oxygen species scavenger, with reported anti-tumor and anti-inflammatory activity. Curcumin has been shown to attenuate mitochondrial dysfunction, stabilize the cell membrane, stimulate proliferation, and reduce injury severity in adult models of spinal cord injury, cancer, and cardiovascular disease. The role of curcumin in neonatal HIE has not been widely studied due to its low bioavailability and limited aqueous solubility. The aim of this study was to investigate the effect of curcumin treatment in neonatal HIE, including time of administration and dose-dependent effects. Our results indicate that curcumin administration prior to HIE in neonatal mice elevated cell and tissue loss, as well as glial activation compared to HI alone. However, immediate post-treatment with curcumin was significantly neuroprotective, reducing grey and white matter tissue loss, TUNEL+ cell death, microglia activation, reactive astrogliosis, and iNOS oxidative stress when compared to vehicle-treated littermates. This effect was dose-dependent, with 200 μg/g body weight as the optimal dose-regimen, and was maintained when curcumin treatment was delayed by 60 or 120 min post-HI. Cell proliferation measurements showed no changes between curcumin and HI alone, suggesting that the protective effects of curcumin on the neonatal brain following HI are most likely due to curcumin’s anti-inflammatory and antioxidant properties, as seen in the reduced glial and iNOS activity. In conclusion, this study suggests curcumin as a potent neuroprotective agent with potential for the treatment of HIE. The delayed application of curcumin further increases its clinical relevance.

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Protective effects of curcumin against ischemia-reperfusion injury in the liver

Cited by 58 publications

References 125 publications

Effect of curcumin dietary supplementation on growth performance, physiology, carcass characteristics and meat quality in lambs

Effect of curcumin dietary supplementation on growth performance, physiology, carcass characteristics and meat quality in lambs

Cinnamaldehyde protects against rat intestinal ischemia/reperfusion injuries by synergistic inhibition of NF-κB and p53

Curcumin: Novel Treatment in Neonatal Hypoxic-Ischemic Brain Injury

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