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Khadijeh Mousavi

Other affiliations: Shanxi Agricultural University
Bio: Khadijeh Mousavi is an academic researcher from Shiraz University of Medical Sciences. The author has contributed to research in topics: Oxidative stress & Cholestasis. The author has an hindex of 6, co-authored 15 publications receiving 105 citations. Previous affiliations of Khadijeh Mousavi include Shanxi Agricultural University.

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Journal ArticleDOI
TL;DR: Evaluated pathologic effects of cholestasis-associated reproductive toxicity in male and female rats is restrictedly coupled with severe oxidative stress and mitochondrial impairment.

48 citations

Journal ArticleDOI
04 Mar 2021-Stress
TL;DR: It was found that NAC treatment significantly mitigated biomarkers of oxidative stress and alleviated tissue histopathological changes in cirrhotic rats, representing NAC as a potential protective agent with therapeutic capability in cholestasis and its associated complications.
Abstract: Cholestasis is a multifaceted clinical complication. Obstructive jaundice induced by bile duct ligation (BDL) is known as an animal model to investigate cholestasis and its associated complications...

30 citations

Journal ArticleDOI
30 Sep 2020
TL;DR: Tau treatment significantly decreased oxidative stress and improved mitochondrial function in the heart tissue of cirrhotic animals, providing clues for the involvement of mitochondrial impairment and oxidative stress in the pathogenesis of heart injury in BDL rats.
Abstract: Cirrhosis-induced heart injury and cardiomyopathy is a serious consequence of this disease. It has been shown that bile duct ligated (BDL) animals could serve as an appropriate experimental model to investigate heart tissue injury in cirrhosis. The accumulation of cytotoxic chemicals (e.g., bile acids) could also adversely affect the heart tissue. Oxidative stress and mitochondrial impairment are the most prominent mechanisms of bile acid cytotoxicity. Taurine (Tau) is the most abundant non-protein amino acid in the human body. The cardioprotective effects of this amino acid have repeatedly been investigated. In the current study, it was examined whether mitochondrial dysfunction and oxidative stress are involved in the pathogenesis of cirrhosis-induced heart injury. Rats underwent BDL surgery. BDL animals received Tau (50, 100, and 500 mg/kg, i.p.) for 42 consecutive days. A significant increase in oxidative stress biomarkers was detected in the heart tissue of BDL animals. Moreover, it was found that heart tissue mitochondrial indices of functionality were deteriorated in the BDL group. Tau treatment significantly decreased oxidative stress and improved mitochondrial function in the heart tissue of cirrhotic animals. These data provide clues for the involvement of mitochondrial impairment and oxidative stress in the pathogenesis of heart injury in BDL rats. On the other hand, Tau supplementation could serve as an effective ancillary treatment against BDL-associated heart injury. Mitochondrial regulating and antioxidative properties of Tau might play a fundamental role in its mechanism of protective effects in the heart tissue of BDL animals.

26 citations

Journal ArticleDOI
TL;DR: The protective role of BET in the intestine of cirrhotic animals could be attributed to the effect of this compound on oxidative stress and its associated events in enterocytes.

24 citations

Journal ArticleDOI
01 Aug 2020-Biologia
TL;DR: It is suggested that CA supplementation with RT improved muscle function by regulating mitochondrial function and cellular energy metabolism, and could be a promising, supplementary/therapeutic agent against a variety of skeletal muscle-associated complications.
Abstract: Chlorogenic acid (CA), is a polyphenol abundantly found in several foods. Different pharmacological roles of CA, including its effect on body weight, become a subject of research interest. In the current study, the effect of CA supplementation was evaluated on the muscle mitochondria function in an animal model of resistance training (RT). Rats were allotted into control, CA (100 mg/kg) without RT, RT, RT + CA 10 mg/kg, RT + CA 50 mg/kg, and RT + CA 100 mg/kg. It was found that CA supplementation (10, 50, and 100 mg/kg, gavage, 56 consecutive days) significantly improved muscle strength and mitochondrial function, especially when it was co-administered with the RT program. The present findings suggest that CA supplementation with RT improved muscle function by regulating mitochondrial function and cellular energy metabolism. Therefore, CA could be a promising, supplementary/therapeutic agent against a variety of skeletal muscle-associated complications.

24 citations


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Journal ArticleDOI
TL;DR: The multiple GSH functions will be described, as well as the importance of GSH compartmentalization into distinct subcellular pools and inter-organ transfer, and the close relationship existing between GSH content and the pathogenesis of liver disease, such as non-alcoholic fatty liver disease (NAFLD, alcoholic liver disease) and chronic cholestatic injury.
Abstract: Glutathione (GSH), a tripeptide particularly concentrated in the liver, is the most important thiol reducing agent involved in the modulation of redox processes. It has also been demonstrated that GSH cannot be considered only as a mere free radical scavenger but that it takes part in the network governing the choice between survival, necrosis and apoptosis as well as in altering the function of signal transduction and transcription factor molecules. The purpose of the present review is to provide an overview on the molecular biology of the GSH system; therefore, GSH synthesis, metabolism and regulation will be reviewed. The multiple GSH functions will be described, as well as the importance of GSH compartmentalization into distinct subcellular pools and inter-organ transfer. Furthermore, we will highlight the close relationship existing between GSH content and the pathogenesis of liver disease, such as non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), chronic cholestatic injury, ischemia/reperfusion damage, hepatitis C virus (HCV), hepatitis B virus (HBV) and hepatocellular carcinoma. Finally, the potential therapeutic benefits of GSH and GSH-related medications, will be described for each liver disorder taken into account.

66 citations

Journal ArticleDOI
TL;DR: Taurine is regarded as a cytoprotective molecule due to its ability to sustain normal electron transport chain, maintain glutathione stores, upregulate anti-oxidant responses, increase membrane stability, eliminate inflammation and prevent calcium accumulation as mentioned in this paper.
Abstract: Taurine is a fundamental mediator of homeostasis that exerts multiple roles to confer protection against oxidant stress. The development of hypertension, muscle/neuro‑​associated disorders, hepatic cirrhosis, cardiac dysfunction and ischemia/reperfusion are examples of some injuries that are linked with oxidative stress. The present review gives a comprehensive description of all the underlying mechanisms of taurine, with the aim to explain its anti‑oxidant actions. Taurine is regarded as a cytoprotective molecule due to its ability to sustain normal electron transport chain, maintain glutathione stores, upregulate anti‑oxidant responses, increase membrane stability, eliminate inflammation and prevent calcium accumulation. In parallel, the synergistic effect of taurine with other potential therapeutic modalities in multiple disorders are highlighted. Apart from the results derived from research findings, the current review bridges the gap between bench and bedside, providing mechanistic insights into the biological activity of taurine that supports its potential therapeutic efficacy in clinic. In the future, further clinical studies are required to support the ameliorative effect of taurine against oxidative stress.

45 citations

Journal ArticleDOI
TL;DR: Findings indicated that an imbalance in the oxidant-antioxidant system, mitochondrial impairment, and the autophagic process, through inhibition of mTOR, dependent and independent pathways, and Bcl-2, as well as activation of AMPK/PI3K/Beclin1/LC3 routes, could play a pivotal role in As-induced reproductive toxicity through ovarian dysfunction in females.

39 citations

01 Jun 2016
TL;DR: A significant amount of data from animal models of liver disease indicates that administration of betaine can halt and even reverse progression of the disruption of liver function, and the accumulated data indicate that carefully controlled additional investigations in humans are merited.
Abstract: Background Betaine is the trimethyl derivative of glycine and is normally present in human plasma due to dietary intake and endogenous synthesis in liver and kidney. Betaine is utilized in the kidney primarily as an osmoprotectant, whereas in the liver its primary role is in metabolism as a methyl group donor. In both organs, a specific betaine transporter mediates cellular uptake of betaine from plasma. The abundance of both betaine and the betaine transporter in liver greatly exceeds that of other organs. Scope of review The remarkable contributions of betaine to normal human and animal health are summarized together with a discussion of the mechanisms and potential beneficial effects of dietary betaine supplements on liver disease. Major conclusions A significant amount of data from animal models of liver disease indicates that administration of betaine can halt and even reverse progression of the disruption of liver function. Betaine is well-tolerated, inexpensive, effective over a wide range of doses, and is already used in livestock feeding practices. General significance The accumulated data indicate that carefully controlled additional investigations in humans are merited. The focus should be on the long-term use of betaine in large patient populations with liver diseases characterized by development of fatty liver, especially non-alcoholic fatty liver disease and alcoholic liver disease.

36 citations

Journal ArticleDOI
TL;DR: In this paper , the effect of trimethyltin chloride (TMT) on mouse kidneys and its related mechanism were studied by taking TMT mouse with drinking water as a model, and the results showed that oxidative stress was activated (MDA,SOD,CAT,T-AOC), released ROS, activated NF-κB pathway,activated inflammasome (NLRP3,Caspase-1,ASC), and inflamma-secreted inflammatory factors (IL-1β).

33 citations