Mitochondria protection as a mechanism underlying the hepatoprotective effects of glycine in cholestatic mice

Heidari, Reza; Ghanbarinejad, Vahid; Mohammadi, Hamidreza; Ahmadi, Asrin; Ommati, Mohammad Mehdi; Abdoli, Narges; Aghaei, Fatemeh; Esfandiari, Athena; Azarpira, Negar; Niknahad, Hossein

doi:10.1016/j.biopha.2017.10.166

Cited by 62 publications

(53 citation statements)

References 72 publications

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“…The open field arena was equipped with a webcam (2.0 Megapixel, Gigaware, UK) and animals activity was monitored and recorded from a separate room. Rats’ behavior was recorded for fifteen minutes, and the total number of crossed squares was counted (total locomotion) [ 44 ].…”

Section: Methodsmentioning

confidence: 99%

Taurine supplementation abates cirrhosis-associated locomotor dysfunction

Heidari

Jamshidzadeh

Ghanbarinejad

et al. 2018

ceh

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Aim of the studyHepatic encephalopathy and hyperammonemia is a clinical complication associated with liver cirrhosis. The brain is the target organ for ammonia toxicity. Ammonia-induced brain injury is related to oxidative stress, locomotor activity dysfunction, and cognitive deficit, which could lead to permanent brain injury, coma and death if not appropriately managed. There is no promising pharmacological intervention against cirrhosis-associated brain injury. Taurine (TAU) is one of the most abundant amino acids in the human body. Several physiological and pharmacological roles have been attributed to TAU. TAU may act as an antioxidant and is an excellent neuroprotective agent. This study aimed to evaluate the effect of TAU supplementation on cirrhosis-associated locomotor activity disturbances and oxidative stress in the brain.Material and methodsRats underwent bile duct ligation (BDL) surgery, and plasma and brain ammonia level, plasma biochemical parameters, and rats’ locomotor function were monitored. Furthermore, brain tissue markers of oxidative stress were assessed.ResultsIt was found that plasma and brain ammonia was increased, and markers of liver injury were significantly elevated in the cirrhotic group. Impaired locomotor activity was also evident in BDL rats. Moreover, an increase in brain tissue markers of oxidative stress was detected in the brain of cirrhotic animals. It was found that TAU supplementation (50, 100, and 200 mg/kg, gavage) alleviated brain tissue markers of oxidative stress and improved animals’ locomotor activity.ConclusionsThese data suggest that TAU is a potential protective agent against cirrhosis-associated brain injury.

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Section: Methodsmentioning

confidence: 99%

Taurine supplementation abates cirrhosis-associated locomotor dysfunction

Heidari

Jamshidzadeh

Ghanbarinejad

et al. 2018

ceh

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“…These indications are fully consistent with reports on the increased enrollment of glycolytic energy metabolism, which sustains energy production to compensate for mitochondrial dysfunction. They are also in keeping with the occurrence of mitochondria dysfunction and oxidative stress in the development of injury in hepatic and extrahepatic sites in cholestasis [ 4 , 11 , 12 ].…”

Section: Discussionmentioning

confidence: 67%

“…BDL induces a cascade of an ensuing, dynamic series of acute and chronic injuries [ 5 , 8 , 9 ]. The early effects on liver bio-metabolic features may include dysfunction of mitochondria and oxidative stress [ 10 , 11 , 12 ] and activation of the inflammatory response of the liver tissue, as well as an increase in the proliferation of hepatocellular or biliary epithelial cells and in mediators of collagen production and fibrosis. Fibrosis, in turn, may well progress to cirrhosis.…”

Section: Introductionmentioning

confidence: 99%

Serum and Hepatic Autofluorescence as a Real-Time Diagnostic Tool for Early Cholestasis Assessment

Croce

Bottiroli

Pasqua

et al. 2018

IJMS

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While it is well established that various factors can impair the production and flow of bile and lead to cholestatic disease in hepatic and extrahepatic sites, an enhanced assessment of the biomarkers of the underlying pathophysiological mechanisms is still needed to improve early diagnosis and therapeutic strategies. Hence, we investigated fluorescing endogenous biomolecules as possible intrinsic biomarkers of molecular and cellular changes in cholestasis. Spectroscopic autofluorescence (AF) analysis was performed using a fiber optic probe (366 nm excitation), under living conditions and in serum, on the livers of male Wistar rats submitted to bile duct ligation (BDL, 24, 48, and 72 h). Biomarkers of liver injury were assayed biochemically. In the serum, AF analysis distinctly detected increased bilirubin at 24 h BDL. A continuous, significant increase in red-fluorescing porphyrin derivatives indicated the subversion of heme metabolism, consistent with an almost twofold increase in the serum iron at 72 h BDL. In the liver, changes in the AF of NAD(P)H and flavins, as well as lipopigments, indicated the impairment of mitochondrial functionality, oxidative stress, and the accumulation of oxidative products. A serum/hepatic AF profile can be thus proposed as a supportive diagnostic tool for the in situ, real-time study of bio-metabolic alterations in bile duct ligation (BDL) in experimental hepatology, with the potential to eventually translate to clinical diagnosis.

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“…*P < 0.05 and **P < 0.01 vs. the control group; # P < 0.05 and ## P < 0.01 vs. the TCDC group; @ P < 0.05 and @@ P < 0.01 vs. the TCDC+ forsythoside-A group;^P < 0.05 and^^P < 0.01 vs. the TCDC+ emodin group; & P < 0.05 and && P < 0.01 vs. the TCDC+ chlorogenic acid group. (Heidari et al, 2018). As reported in a previous study, the mitochondrial pathway plays a crucial role in cell apoptosis (Gibson and Davids, 2015).…”

Section: Hepatocytic Levels Of Apoptosis-related Proteins Involved Inmentioning

confidence: 67%

Li-Dan-He-Ji Improves Infantile Cholestasis Hepatopathy Through Inhibiting Calcium-Sensing Receptor-Mediated Hepatocyte Apoptosis

et al. 2020

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in the intracellular calcium concentration ([Ca 2+ ] i ) and ROS levels and attenuated the dissipation of the mitochondria membrane potential in the TCDC-induced primary hepatocytes. The opposite results were obtained from the TCDC-induced primary hepatocytes treated with an agonist of CaSR (GdCl 3 ) plus forsythoside-A, emodin or chlorogenic acid. Based on the results from in vivo and in vitro studies, LDHJ functions as an antagonist of CaSR to regulate hepatocyte apoptosis in cholestasis through the mitochondrial pathway and mitogen-activated protein kinase pathway.

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Mitochondria protection as a mechanism underlying the hepatoprotective effects of glycine in cholestatic mice

Cited by 62 publications

References 72 publications

Taurine supplementation abates cirrhosis-associated locomotor dysfunction

Taurine supplementation abates cirrhosis-associated locomotor dysfunction

Serum and Hepatic Autofluorescence as a Real-Time Diagnostic Tool for Early Cholestasis Assessment

Li-Dan-He-Ji Improves Infantile Cholestasis Hepatopathy Through Inhibiting Calcium-Sensing Receptor-Mediated Hepatocyte Apoptosis

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