Allicin ameliorates renal ischemia/reperfusion injury via inhibition of oxidative stress and inflammation in rats

Shan, Yungang; Chen, Deqing; Hu, Bo; Xu, Guangtao; Li, Wanlu; Jin, Yufeng; Jin, Xiuhui; Jin, Xin; Jin, Limin

doi:10.1016/j.biopha.2021.112077

Cited by 41 publications

(24 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additionally, histological examination showed that the renal I/R group displayed severe histological alterations, indicating renal injury due to renal ischemia-reperfusion (I/R). Previous studies showed that renal I/R increased renal function markers [ 2 , 5 , 16 ] and several histological alterations [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, Nrf2, HO-1, and NQO-1 gene and protein expression were slightly escalated in animals that experienced renal I/R. Numerous studies indicated that renal ischemia/reperfusion induces nuclear translocation of Nrf2 [ 7 , 16 ], with subsequent augmented levels of HO-1, SOD, and NQO-1 [ 2 , 5 , 16 ].…”

Section: Discussionmentioning

confidence: 99%

“…Earlier studies demonstrated that the expression of TLR4 and its downstream factors were significantly amplified, and the nuclear translocation of NF-κB p65 was increased after the renal I/R [ 16 ]. Additionally, pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 were significantly increased in IRI rats [ 2 , 5 , 16 ], and anti-inflammatory cytokine IL-10 was lowered in renal I/R [ 5 ].…”

Section: Discussionmentioning

confidence: 99%

“…The underlying pathophysiological mechanisms involved in renal I/R induced-injury include releasing reactive oxygen species (ROS), generating pro-inflammatory mediators, calcium overload, and activating apoptotic genes [ 4 ]. The ROS detrimental outcome on renal tissues has been considered fundamental in renal injury pathophysiological processes [ 5 ]. Oxygen radicals manufactured after ischemia/reperfusion can cause lipid peroxidation and destroy cell and organelle membranes, disturbing renal tissue structure and function.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Renal Ischemia/Reperfusion Mitigation via Geraniol: The Role of Nrf-2/HO-1/NQO-1 and TLR2,4/MYD88/NFκB Pathway

2022

View full text Add to dashboard Cite

Background: Renal ischemia/reperfusion injury is a clinically recurrent event during kidney transplantation. Geraniol is a natural monoterpene essential oil component. This study aimed to inspect geraniol’s reno-protective actions against renal I/R injury with further analysis of embedded mechanisms of action through scrutinizing the Nrf-2/HO-1/NQO-1 and TLR2,4/MYD88/NFκB signaling pathways. Methods: Wistar male rats were randomized into five groups: Sham, Sham + geraniol, Renal I/R, and two Renal I/R + geraniol groups representing two doses of geraniol (100 and 200 mg/kg) for 14 days before the renal I/R. Renal I/R was surgically induced by occluding both left and right renal pedicles for 45 min, followed by reperfusion for 24 h. A docking study was performed to anticipate the expected affinity of geraniol towards three protein targets: hTLR4/MD2, hTLR2, and hNrf2/Keap1. Results: Renal I/R rats experienced severely compromised renal functions, histological alteration, oxidative stress status, escalated Nrf-2/HO-1/NQO-1, and amplified TLR2,4/MYD88/NFκB. Geraniol administration ameliorated renal function, alleviated histological changes, and enhanced Nrf-2/HO-1/NQO-1 with a subsequent intensification of antioxidant enzyme activities. Geraniol declined TLR2,4/MYD88/NFκB with subsequent TNF-α, IFN-γ, MCP-1 drop, Bax, caspase-3, and caspase-9 reduction IL-10 and Bcl-2 augmentation. Geraniol exhibited good fitting in the binding sites of the three in silico examined targets. Conclusions: Geraniol might protect against renal I/R via the inhibition of the TLR2,4/MYD88/NFκB pathway, mediating anti-inflammation and activation of the Nrf2 pathway, intervening in antioxidative activities.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Renal Ischemia/Reperfusion Mitigation via Geraniol: The Role of Nrf-2/HO-1/NQO-1 and TLR2,4/MYD88/NFκB Pathway

2022

View full text Add to dashboard Cite

show abstract

“…The protocol was previously described [ 17 – 19 ]. A lysis buffer (Beyotime, Shanghai, China) containing a protease inhibitor cocktail (Millipore, Billerica, Massachusetts, USA) was utilized to isolate proteins from cardiac tissues.…”

Section: Methodsmentioning

confidence: 99%

Honokiol Provides Cardioprotection from Myocardial Ischemia/Reperfusion Injury (MI/RI) by Inhibiting Mitochondrial Apoptosis via the PI3K/AKT Signaling Pathway

Kong

et al. 2022

Cardiovascular Therapeutics

View full text Add to dashboard Cite

Background. Myocardial injury refers to a major complication that occurs in myocardial ischemia/reperfusion injury (MI/RI). Honokiol is a well-recognized active compound extracted from the traditional Chinese herb known as Magnolia officinalis and is utilized in treating different vascular diseases. This research is aimed at examining whether Honokiol might alleviate myocardial injury in an MI/RI model. Methods. Seventy-eight male C57BL/6 mice were categorized randomly into three cohorts including the Sham operation (Sham) cohort, the MI/RI cohort (Con), and the Honokiol cohort ( n = 26 for each cohort). The mice in the Honokiol cohort were treated with Honokiol before MI/RI surgery (0.2 mg/kg/day for 14 days, intraperitoneal), while the mice in the Con cohort were given an intraperitoneal injection with an equivalent volume of vehicle (DMSO) daily in 14 days prior to exposure to MI/RI. After the surgery, creatine kinase- (CK-) MB and cardiac troponin T (cTnT) levels, as well as the infarct area, were measured to assess the degree of myocardial damage. Apoptotic levels were detected using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Electron microscopy was utilized to identify mitochondrial damage. Lastly, the expression levels of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), cleaved caspase-9, cytochrome C (Cyt-C), B cell lymphoma/leukemia-2 (Bcl-2), B cell lymphoma/leukemia-2 associated X (Bax), AKT, p-AKT, PI3K, and p-PI3K were analyzed utilizing western blotting. Results. Honokiol can reduce the MI/RI-induced cTnT and CK-MB levels, apoptosis index, and mitochondrial swelling in cardiomyocytes via activating the PI3K/AKT signaling pathway. Conclusion. Honokiol provides cardiac protection from MI/RI by suppressing mitochondrial apoptosis through the PI3K/AKT signaling pathway.

show abstract

Annexin-A5 monomer as a membrane repair agent for the treatment of renal ischemia-reperfusion injury

Dong,

Jia,

Kang

et al. 2024

Mol Biol Rep

View full text Add to dashboard Cite

Background: Renal ischemia-reperfusion injury (IRI) is one of the causes of acute kidney injury. Annexin A5 (AnxA5) as a calcium-dependent cell membrane binding protein has shown good protective effects in various organ IRI models. This study explored the therapeutic effect of exogenous AnxA5 monomer protein on renal IRI and its potential mechanism.Methods: In vivo, different doses of AnxA5 were injected intravenously to treat bilateral renal IRI models in SD rats. This model con rms the protective effect of AnxA5 on the structure and function of the kidneys. In vitro, HK-2, the renal tubular epithelial cells, was subjected to hypoxia for 12 hours, followed by restoration of normal oxygen supply to simulate IRI. In vitro experiments have demonstrated the mechanism of action of AnxA5 by measuring cell activity and permeability. The comparison of the mutant AnxA5 protein M23 and the application of calcium-free culture medium further validated the protective effect of AnxA5 by forming a network structure.Results: In vivo, AnxA5 monomer improved kidney function damage caused by IRI and prevented the deterioration of the pathological structure. In vitro, AnxA5 protected cell viability, reduced cell membrane permeability, and inhibited cell apoptosis induced by IRI treatment. However, AnxA5 lost its protective effect in the calcium-free culture medium and the M23 that lack the ability of forming a two-dimensional network structure could not reduce cell membrane permeability and lost its protective effect on cell viability, indicating that the formation of a two-dimensional network structure of AnxA5 is critical to the repair of the cell membrane.Conclusions: Exogenous AnxA5 monomer could prevent renal IRI by binding to the damaged renal tubular epithelial cell membrane, forming a two-dimensional network structure to maintain cell membrane integrity, and ultimately prevent cell death.

show abstract

Allicin ameliorates renal ischemia/reperfusion injury via inhibition of oxidative stress and inflammation in rats

Cited by 41 publications

References 39 publications

Renal Ischemia/Reperfusion Mitigation via Geraniol: The Role of Nrf-2/HO-1/NQO-1 and TLR2,4/MYD88/NFκB Pathway

Renal Ischemia/Reperfusion Mitigation via Geraniol: The Role of Nrf-2/HO-1/NQO-1 and TLR2,4/MYD88/NFκB Pathway

Honokiol Provides Cardioprotection from Myocardial Ischemia/Reperfusion Injury (MI/RI) by Inhibiting Mitochondrial Apoptosis via the PI3K/AKT Signaling Pathway

Annexin-A5 monomer as a membrane repair agent for the treatment of renal ischemia-reperfusion injury

Contact Info

Product

Resources

About