Allicin mitigates hepatic injury following cyclophosphamide administration via activation of Nrf2/ARE pathways and through inhibition of inflammatory and apoptotic machinery

Sun, Dongsheng; Sun, Chen; Qiu, Gongcai; Yao, Lei; Yu, Jian; Sberi, Hassan Al; Fouda, Manar S.; Othman, Mohamed S.; Lokman, Maha S.; Kassab, Rami B.; Moneim, Ahmed E. Abdel

doi:10.1007/s11356-021-13392-w

Cited by 26 publications

(15 citation statements)

References 63 publications

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“…As presented in the current study’s results, CYP induced a significant increase in the IL-1β levels, which is parallel to the findings of previous studies 48 – 50 .…”

Section: Discussionsupporting

confidence: 92%

Protective effects of hesperidin in cyclophosphamide-induced parotid toxicity in rats

Mostafa

Ibrahim

Borai

2023

Sci Rep

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Cyclophosphamide (CYP) is an alkylating agent that is used on a wide range as a treatment of malignancies and autoimmune diseases. Previous studies have shown the promising role of hesperidin (HSP) as an antioxidant agent against various models of toxic agents. The protective effect of the HSP against CYP-induced parotid damage was evaluated in this study. Forty rats (180–200 g) were divided into four equal groups: Group I (received normal saline), Group II (HSP-treated at a dose of 100 mg/kg/day for 7 consecutive days), Group III (CYP-treated at a dose of 200 mg/kg single intraperitoneal injection on the 7th day of the experiment), Group IV (CYP + HSP); HSP-treated at a dose of 100 mg/kg/day for 7 consecutive days and CYP (200 mg/kg) single intraperitoneal injection on the 7th day of the experiment. Afterwards, the oxidative stress and inflammatory markers, the histopathological and immunohistochemical alterations of the parotid tissues in the studied groups were evaluated. CYP intoxication induced a significant parotid tissue injury represented by the elevation in the values of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and decrease in the catalase activity and glutathione peroxidase (GPx). Histologically, extensive histopathological alterations e.g., widely spaced serous acini with irregular shapes and congested blood vessels as well as downregulated ki-67 and alpha-smooth muscle actin (α-SMA) immunoexpression were induced by CYP. HSP administration markedly improved the biochemical and the histopathological studies. We can conclude that HSP elicited protective effects against the CYP-induced parotid toxicity.

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“…As presented in the current study’s results, CYP induced a significant increase in the IL-1β levels, which is parallel to the findings of previous studies 48 – 50 .…”

Section: Discussionsupporting

confidence: 92%

Protective effects of hesperidin in cyclophosphamide-induced parotid toxicity in rats

Mostafa

Ibrahim

Borai

2023

Sci Rep

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“…[14][15][16] Additionally, it can help alleviate liver damage in various hepatic diseases. 17,18 Hence, we hypothesized that allicin might protect against hepatic I/R injury. We discovered that allicin ameliorated hepatic I/R injury in mice via the PPARγ-IRAK-M-TLR4 signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

Allicin attenuated hepatic ischemia/reperfusion injury in mice by regulating PPARγ-IRAK-M-TLR4 signal pathway

Huang

Gong

et al. 2022

Food Funct.

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“…In the present study, we noticed that the allicin prevented the LPSinduced oxidative stress, which may be considered as a key mechanism that participates in preventing barrier damage of the IPEC-J2 cell monolayers. Previous studies reported that allicin mitigates hepatic injury (47), hepatotoxicity (48), and cardiac hypertrophy (49) via activating Nrf-2 pathways. In the present study, allicin ranging from safe concentrations was verified to regulate the Nrf2 and HO-1 mRNA levels both in dose-dependent and time-dependent manners.…”

Section: Discussionmentioning

confidence: 99%

Allicin Improves Intestinal Epithelial Barrier Function and Prevents LPS-Induced Barrier Damages of Intestinal Epithelial Cell Monolayers

et al. 2022

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Gut barrier disruption is the initial pathogenesis of various diseases. We previously reported that dietary allicin improves tight junction proteins in the endoplasmic reticulum stressed jejunum. However, whether the allicin benefits the gut barrier within mycotoxin or endotoxin exposure is unknown. In the present study, IPEC-J2 cell monolayers within or without deoxynivalenol (DON) or lipopolysaccharide (LPS) challenges were employed to investigate the effects of allicin on intestinal barrier function and explore the potential mechanisms. Results clarified that allicin at 2 μg/mL increased the viability, whereas the allicin higher than 10 μg/mL lowered the viability of IPEC-J2 cells via inhibiting cell proliferation. Besides, allicin increased trans-epithelial electric resistance (TEER), decreased paracellular permeability, and enhanced ZO-1 integrity of the IPEC-J2 cell monolayers. Finally, allicin supplementation prevented the LPS-induced barrier damages via activating Nrf2/HO-1 pathway-dependent antioxidant system. In conclusion, the present study strongly confirmed allicin as an effective nutrient to improve intestinal barrier function and prevent bacterial endotoxin-induced barrier damages.

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Allicin mitigates hepatic injury following cyclophosphamide administration via activation of Nrf2/ARE pathways and through inhibition of inflammatory and apoptotic machinery

Cited by 26 publications

References 63 publications

Protective effects of hesperidin in cyclophosphamide-induced parotid toxicity in rats

Protective effects of hesperidin in cyclophosphamide-induced parotid toxicity in rats

Allicin attenuated hepatic ischemia/reperfusion injury in mice by regulating PPARγ-IRAK-M-TLR4 signal pathway

Allicin Improves Intestinal Epithelial Barrier Function and Prevents LPS-Induced Barrier Damages of Intestinal Epithelial Cell Monolayers

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