Mitochondrial dynamics in the mouse liver infected by Schistosoma mansoni

Chen, Tina Tu Wen; Wu, Lawrence Shih Hsin; Hsu, Paul Wei Che; Pang, Cheng‐Yoong; Lee, Kin Mu; Cheng, Po Ching; Peng, Shih-Yi

doi:10.1016/j.actatropica.2015.04.004

Cited by 13 publications

(5 citation statements)

References 35 publications

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“…In the present study, the S. japonicum infection was found to induce mitochondrial dysfunction and reduce mitochondrial biogenesis, as shown by the decrease in the mitochondrial membrane potential (Δφm) and the decrease in PGC-1α expression. Similarly, a recent study revealed that having the S. mansoni infection for 8 weeks induces mitochondria damage, and a decrease in the expression of genes involved in mitochondrial functional and biogenesis was noted [14]. In the present study, the inhibitory effects of S. japonicum on Δφm and PGC-1α expression were attenuated after 3 weeks of RSV treatment in the mice with S. japonicum infection.…”

Section: Discussionsupporting

confidence: 75%

“…Our previous study reported that the S. mansoni infection changes the mitochondrial morphology and promotes mitochondrial fragmentation in the mouse liver. In addition, it also affects mitochondrial function and attenuates mitochondrial membrane potential [14]. Furthermore, the S. mansoni infection was found to disrupt the mitochondrial dynamics of the mouse liver and induce mitochondrial fission [14].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, it also affects mitochondrial function and attenuates mitochondrial membrane potential [14]. Furthermore, the S. mansoni infection was found to disrupt the mitochondrial dynamics of the mouse liver and induce mitochondrial fission [14]. Based on these results, it is possible that drugs that target mitochondrial morphology and function as well as the proteins involved in mitochondrial networks may present useful targets for the treatment of schistosomiasis.…”

Section: Introductionmentioning

confidence: 99%

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Improvement of Mitochondrial Activity and Fibrosis by Resveratrol Treatment in Mice with Schistosoma japonicum Infection

et al. 2019

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Schistosomiasis caused by Schistosoma japonicum is a major parasitic disease in the People’s Republic of China. Liver fibrosis is the main pathological mechanism of schistosomiasis, and it is also the major lesion. The common drug used for its treatment, praziquantel (PZQ), does not have a marked effect on liver fibrosis. Resveratrol (RSV), which is an antioxidant, improves mitochondrial function and also attenuates liver fibrosis. The combination of PZQ and RSV has been found to have a synergistic antischistosomal effect on Schistosoma mansoni; additionally, the activity of PZQ is enhanced in the presence of RSV. Here, we examine the therapeutic effects of RSV on the S. japonicum infection in a mouse model, and we investigate RSV as a novel therapeutic agent for mitochondrial function and schistosomiasis-associated liver fibrosis (SSLF). Mitochondrial membrane potential was examined using flow cytometry analysis. The expression of the mitochondrial biogenesis genes PGC-α and fibrosis-associated genes collagen I, collagen III and α-SMA were examined using western blot analysis. Fibrosis-associated histological changes were examined using Masson trichrome staining. Additionally, the effects of RSV on S. japonicum adult worms were examined using scanning electron microscopy and transmission electron microscopy. RSV treatment improved mitochondrial function by increasing membrane potential and increasing PGC-α expression (mitochondrial biogenesis). Further, RSV attenuated liver injury, including liver scarring, by decreasing collagen deposition and the extent of fibrosis, based on the decrease in expression of the fibrosis-related genes. RSV also decreased the adult worm count and caused considerable physical damage to the worm. These results indicate that RSV upregulates mitochondrial biogenesis and inhibits fibrosis. RSV may have potential as a therapeutic target for the treatment of fibrosis in schistosomiasis.

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Section: Discussionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Improvement of Mitochondrial Activity and Fibrosis by Resveratrol Treatment in Mice with Schistosoma japonicum Infection

et al. 2019

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“…8 mL red blood cell (RBC) lysis buffer (0.15 M NH 4 Cl, 1 mM KHCO 3 , 0.1 mM Na 2 EDTA; pH 7.2–7.4) were added to lysed the erythrocytes. After centrifugation at 250× g for 5 min, cells were resuspended in 5% FBS-containing PBS and were passed through a 70 μm nylon mesh cell strainer (Corning, Inc., Corning, NY, USA) [ 89 , 90 ].…”

Section: Methodsmentioning

confidence: 99%

Ameliorative effects of Schisandrin B on Schistosoma mansoni-induced hepatic fibrosis in vivo

2021

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Schistosomiasis is second only to malaria as the most devastating parasitic disease in the world. It is caused by the helminths Schistosoma mansoni (S. mansoni), S. haematobium, or S. japonicum. Typically, patients with schistosomiasis suffer from symptoms of liver fibrosis and hepatosplenomegaly. Currently, patients were treated with praziquantel. Although praziquantel effectively kills the worm, it cannot prevent re-infection or resolve liver fibrosis. Also, current treatment options are not ample to completely cure liver fibrosis and splenic damages. Moreover, resistance of praziquantel has been reported in vivo and in vitro studies. Therefore, finding new effective treatment agents is urgently needed. Schisandrin B (Sch B) of Schisandra chinensis has been shown to protect against different liver injuries including fatty liver disease, hepatotoxicity, fibrosis, and hepatoma. We herein investigate the potential of using Sch B to treat S. mansoni-induced liver fibrosis. Results from the present study demonstrate that Sch B is beneficial in treating S. mansoni-induced liver fibrosis and splenic damages, through inhibition of inflammasome activation and apoptosis; and aside from that regulates host immune responses. Besides, Sch B treatment damages male adult worm in the mice, consequently helps to reduce egg production and lessen the parasite burden.

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“…Here, we aimed to examine whether ROS and NF-κB (p65) expression elicited other types of inflammasome activation in S. mansoni -infected mouse livers. A previous study indicated that Hepatitis C virus (HCV), Ribonucleic acid (RNA) activated the NLRP3 inflammasome in a ROS-dependent manner in infected hepatic HuH-7 cells (Chen et al ., 2014). To demonstrate whether schistosomal components activate this inflammasome, we investigated inflammasome activation in HuH-7 cells treated with different doses of SEA for 12 and 24 h. In addition to the previous findings that S. mansoni infection induced apoptosis and mitochondrial dysfunction in mouse livers, we report here that the AIM2 inflammasome is also triggered by exposure to schistosomal antigen.…”

Section: Introductionmentioning

confidence: 99%

Activation of the NLRP3 and AIM2 inflammasomes in a mouse model ofSchistosoma mansoniinfection

et al. 2019

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Schistosomiasis is an inflammatory disease that occurs when schistosome species eggs are deposited in the liver, resulting in fibrosis and portal hypertension. Schistosomes can interact with host inflammasomes to elicit host immune responses, leading to mitochondrial damage, generation of high levels of reactive oxygen species (ROS) and activation of apoptosis during inflammation. This study aims to examine whether ROS and NF-κB (p65) expression elicited other types of inflammasome activation in Schistosoma mansoni-infected mouse livers. We examine the relationship between inflammasome activation, mitochondrial damage and ROS production in mouse livers infected with S. mansoni. We demonstrate a significant release of ROS and superoxides and increased NF-κB (p65) in S. mansoni-infected mouse livers. Moreover, activation of the NLRP3 and AIM2 inflammasomes was triggered by S. mansoni infection. Stimulation of HuH-7 hepatocellular carcinoma cells with soluble egg antigen induced activation of the AIM2 inflammasome pathway. In this study, we demonstrate that S. mansoni infection promotes both NLRP3 and AIM2 inflammasome activation.

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Mitochondrial dynamics in the mouse liver infected by Schistosoma mansoni

Cited by 13 publications

References 35 publications

Improvement of Mitochondrial Activity and Fibrosis by Resveratrol Treatment in Mice with Schistosoma japonicum Infection

Improvement of Mitochondrial Activity and Fibrosis by Resveratrol Treatment in Mice with Schistosoma japonicum Infection

Ameliorative effects of Schisandrin B on Schistosoma mansoni-induced hepatic fibrosis in vivo

Activation of the NLRP3 and AIM2 inflammasomes in a mouse model ofSchistosoma mansoniinfection

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