Mechanistic evaluation of AMPK/SIRT1/FXR signaling axis, inflammation, and redox status in thioacetamide‐induced liver cirrhosis: The role of<i>Cichorium intybus</i>linn (chicory)‐supplemented diet

Keshk, Walaa Arafa; Soliman, Nema A.; Ali, Darin Abd-Elaziz; Elseady, Walaa S.

doi:10.1111/jfbc.12938

Cited by 26 publications

(20 citation statements)

References 38 publications

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“…Furthermore, AMPK, as an important protein kinase in the process of cell energy metabolism, can regulate Sirt1 activity and reduce the expression of in ammatory genes by activating AMPK, thus inhibiting the in ammatory response [44,45]. In addition, the reported study showed that TST can protect the acute liver injury by inhibiting NF-κB expression [46,47]. More importantly, it was reported that the activation of AMPK/Sirt1 could inhibited MIRI through alleviate in ammation reaction [32][33][34][35], which is very important for MIRI therapy in clinic.…”

Section: Discussionmentioning

confidence: 96%

Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

Zhang

Wang

Tang

et al. 2020

Preprint

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BackgroundTo investigate the effect and possible mechanisms of total saponins from Trillium Tschonoskii Maxim. (TST) on myocardial ischemia reperfusion injury in rat.Methods and ResultsRats were pre-treated with TST in 100 and 200 mg/kg, respectively. After 14 days intragastric administration, the model of myocardial ischemia-reperfusion injury was established by ligation of the left anterior descending coronary artery for 30 min and then releasing the ligated artery for 120 min. The hemodynamic indexes, anti-oxidation index, and the anti-inflammation factors were detected. Pathological changes in myocardia tissue were observed by H&E staining. Apoptosis protein expression of caspase 3, 9, 12, AMPK, phosphorylation AMPK (p-AMPK) and Sirt1 was detected by Western blot. Pretreating the rats with TST dramatically decreased the levels of MDA, TNF-α, IL-6 and IL-1β, increased the levels of SOD and GSH-Px, and the apoptosis protein expression were all significantly decreased. In addition, the protein expression of p-AMPK and Sirt1 were markedly increased in TST pre-treated group. Furthermore, TST pre-treatment also improved the histopathological changes.ConclusionTST protect the myocardium by reducing the levels of inflammation factors, peroxides and cell apoptosis, increasing the anti-oxidase, and improving the pathological changes. The possible mechanism maybe through the activating of the AMPK/Sirt1 signaling pathway.

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Section: Discussionmentioning

confidence: 96%

Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

Zhang

Wang

Tang

et al. 2020

Preprint

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“…Furthermore, it is known that CREB can activate autophagy genes via the Farnesoid X receptor (FXR)/CREB signaling pathway whereby FXR inhibits CREB activation ( 61 – 63 ). By its turn, AMPK inhibits FXR and thus increases CREB activation ( 64 , 65 ). Regarding BDNF, it was shown that increased levels of BDNF were associated with inhibition of autophagy ( 66 ).…”

Section: Discussionmentioning

confidence: 99%

Sildenafil Alleviates Murine Experimental Autoimmune Encephalomyelitis by Triggering Autophagy in the Spinal Cord

et al. 2021

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Multiple Sclerosis (MS) is a neuroinflammatory and chronic Central Nervous System (CNS) disease that affects millions of people worldwide. The search for more promising drugs for the treatment of MS has led to studies on Sildenafil, a phosphodiesterase type 5 Inhibitor (PDE5I) that has been shown to possess neuroprotective effects in the Experimental Autoimmune Encephalomyelitis (EAE), an animal model of MS. We have previously shown that Sildenafil improves the clinical score of EAE mice via modulation of apoptotic pathways, but other signaling pathways were not previously covered. Therefore, the aim of the present study was to further investigate the effects of Sildenafil treatment on autophagy and nitrosative stress signaling pathways in EAE. 24 female C57BL/6 mice were divided into the following groups: (A) Control - received only water; (B) EAE - EAE untreated mice; (C) SILD - EAE mice treated with 25mg/kg of Sildenafil s.c. The results showed that EAE mice presented a pro-nitrosative profile characterized by high tissue nitrite levels, lowered levels of p-eNOS and high levels of iNOS. Furthermore, decreased levels of LC3, beclin-1 and ATG5, suggests impaired autophagy, and decreased levels of AMPK in the spinal cord were also detected in EAE mice. Surprisingly, treatment with Sildenafil inhibited nitrosative stress and augmented the levels of LC3, beclin-1, ATG5, p-CREB and BDNF and decreased mTOR levels, as well as augmented p-AMPK. In conclusion, we propose that Sildenafil alleviates EAE by activating autophagy via the eNOS-NO-AMPK-mTOR-LC3-beclin1-ATG5 and eNOS-NO-AMPK-mTOR-CREB-BDNF pathways in the spinal cord.

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“…TAA can induce OS, inflammation, and lipid peroxidation to cause liver damage [ 31 ]. Notably, OS was reported to play an essential role in the pathogenesis of TAA-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

Effect of Uncaria rhynchophylla against Thioacetamide-Induced Acute Liver Injury in Rat

Shin

Kim

Lee

et al. 2021

Canadian Journal of Gastroenterology and Hepatology

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Both oxidative stress (OS) and inflammation are two fundamental pathological processes of acute liver injury (ALI). The current work is to investigate the effect and possible mechanism of Uncaria rhynchophylla (UR) on thioacetamide- (TAA-) induced ALI in rats. UR (100 and 200 mg/kg) was orally administrated with TAA (200 mg/kg of bodyweight, intraperitoneal injection) for 3 consecutive days. ALI was confirmed using histological examination and the factors associated with OS and liver function activity measured in serum. Moreover, expressions of inflammation and collagen-related proteins were measured by the Western blot analysis. Myeloperoxidase (MPO), which mediates OS in the ALI control group, was manifested by a significant rise compared with the normal group. UR significantly reduced AST, ALT, and ammonia levels in serum. The nuclear factor-κB (NF-κB) activation induced by TAA led to increase both inflammatory mediators and cytokines. Whereas, UR administration remarkably suppressed such an overexpression. UR supplementation improved matrix metalloproteinases (MMPs) such as MMP-1, -2, and -8. In contrast, tissue inhibitors of metalloproteinases- (TIMP-) 1 level increased significantly by UR treatment. In addition, the histopathological analysis showed that the liver tissue lesions were improved obviously by UR treatment. UR may ameliorate the effects of TAA-induced ALI in rats by suppressing both OS through MPO activation and proinflammatory factors through NF-κB activation. In conclusion, UR exhibited a potent hepatoprotective effect on ALI through the suppression of OS.

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Mechanistic evaluation of AMPK/SIRT1/FXR signaling axis, inflammation, and redox status in thioacetamide‐induced liver cirrhosis: The role ofCichorium intybuslinn (chicory)‐supplemented diet

Cited by 26 publications

References 38 publications

Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

Total saponins from Trillium Tschonoskii Maxim alleviate myocardial ischemia reperfusion injury in rat

Sildenafil Alleviates Murine Experimental Autoimmune Encephalomyelitis by Triggering Autophagy in the Spinal Cord

Effect of Uncaria rhynchophylla against Thioacetamide-Induced Acute Liver Injury in Rat

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