Effect of praziquantel on hepatic fibrosis in experimental Schistosomiasis mansoni

El-Badrawy, N.M.; Hassanein, Hanaa; Botros, Sanaa S.; Nagy, Faten; Abdallah, Nadia M.; Herbage, D.

doi:10.1016/0014-4800(88)90029-9

Cited by 18 publications

(12 citation statements)

References 21 publications

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“…There were many researches that demonstrated the reversibility of inflammation and liver fibrosis after praziquantel treatment of schistosome infection in animal models (Morcos et al 1985;el-Badrawy et al 1988;Barros et al 2009). In addition, in human beings, praziquantel administration also can reverse hepatic fibrosis in most of patients with schistosomiasis, especially in the early stage.…”

Section: Discussionmentioning

confidence: 98%

Effect of praziquantel prolonged administration on granuloma formation around Schistosoma japonicum eggs in lung of sensitized mice

Huang

et al. 2011

Parasitol Res

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Schistosomiasis remains a major public health problem and it is an immune disease. The schistosome egg is the primary parasite factor responsible for the overt disease. The eggs release the soluble antigen, which induces intensive tissue reaction, a granulomatous reaction to the eggs. If granuloma formation could be suppressed, overt disease might not develop. Praziquantel is an effective antischistosomal drug especially for adult worms. However, whether praziquantel has a suppressing effect on granuloma formation around schistosome eggs directly remains unclear. The purpose of the present study was to investigate the effect of praziquantel, especially administered persistently, on granuloma formation around Schistosoma japonicum eggs in the lung of sensitized mice. Thirty-six mice were divided into three groups averagely. Group A was a control group. First, the mice were injected with schistosomal eggs hypodermically in abdomen, and 10 days later injected with schistosomal eggs intravenously via a tail vein. Group B was a praziquantel short administration group. In addition to the injections of schistosomal eggs as the same of Group A, the mice were administered with praziquantel in a daily dose of 300 mg/kg for 3 days, from 1 day before the intravenous injection of the eggs. Group C was a praziquantel prolonged administration group. In addition to the injections of schistosomal eggs as the same of Group A, the mice were administered with praziquantel in a daily dose of 150 mg/kg for 5 days weekly until the mice were sacrificed. Three mice of each group were sacrificed on days 7, 14, 28, and 56, respectively after the intravenous injection of the eggs, and the lung tissues were fixed with formalin and the slices were HE stained. The granulomas containing eggs in their centers were selected, and 25-30 granulomas from the animals of each group were measured at each time period. The mean areas of egg granulomas of each group were calculated, and the neutrophilic granulocytes, eosinocytes, lymphocytes, fibroblasts, and macrophages within the egg granulomas were counted. The mean numbers of them of each group were calculated. All the data of each group were analyzed and compared statistically. On day 56 after the intravenous injection of the eggs, the mean area of schistosomal egg granulomas in group B was (227.4 ± 728.0) × 10(3) μm(2), less than that of [(297.9 ± 153.3) × 10(3) μm(2)] in group A, and the suppression rate was 23.7% (P < 0.05). On days 7, 14, 28, and 56, the mean areas of schistosomal egg granulomas in group C were (575.8 ± 155.6) × 10(3) μm(2), (310.5 ± 854.0) × 10(3) μm(2), (267.7 ± 513.3) × 10(3) μm(2), and (214.9 ± 446.4) × 10(3) μm(2), respectively, significantly less than those of [(692.7 ± 232.6) × 10(3) μm(2), (439.4 ± 165.0) × 10(3) μm(2), (385.7 ± 129.3) × 10(3) μm(2), and (297.9 ± 153.3) × 10(3) μm(2)] in group A. The suppression rates were 16.9%, 29.3%, 30.6%, and 27.9%, respectively (P values <0.05). On day 56, the mean numbers of neutrophilic granulocytes were 11.4 ± 5.0 in group A and 5...

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Section: Discussionmentioning

confidence: 98%

Effect of praziquantel prolonged administration on granuloma formation around Schistosoma japonicum eggs in lung of sensitized mice

Huang

et al. 2011

Parasitol Res

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“…These studies revealed that the schistosomicidal effect of praziquantel depended on the host immunity. More importantly, schistosomiasis‐induced liver fibrosis was effectively ameliorated by praziquantel treatment aimed at killing the schistosomes (Berhe, Myrvang, & Gundersen, ; el‐Badrawy et al, ; Singh, Gerard, Hudson, & Boros, ). However, the antifibrotic effect of praziquantel was attributed to the self‐repair after the death of the schistosomes.…”

Section: Discussionmentioning

confidence: 99%

Praziquantel ameliorates CCl₄‐induced liver fibrosis in mice by inhibiting TGF‐β/Smad signalling via up‐regulating Smad7 in hepatic stellate cells

Liu

Kong

Qiu

et al. 2019

British J Pharmacology

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Background and Purpose: Praziquantel is a schistosomicide, which has been used for more than 30 years due to its efficiency, safety, and mild side effects. Previous studies showed that prolonged treatment with praziquantel suppressed the development of liver fibrosis in mice with schistosomiasis. In this study, we investigated the potential mechanisms underlying the antifibrotic effects of praziquantel. Experimental Approach: To avoid the effect of schistosomicidal activity of praziquantel against liver fibrosis induced by Schistosoma japonicum infection, we established a mouse model of carbon tetrachloride (CCl 4 )-induced liver fibrosis for in vivo studies and used TGF-β1-stimulated human hepatic stellate cell line (LX-2) in addition to other fibroblast-like cell line (MES13) and fibroblast cell line (NIH3T3) in vitro. Western blotting, immunohistochemistry, quantitative real-time PCR, siRNA, and immunofluorescence staining were utilized to assess the expression of key molecules in liver fibrosis and the TGF-β/Smad pathway. Key Results: Praziquantel significantly attenuated CCl 4 -induced liver fibrosis by inhibiting the activation of hepatic stellate cells (HSCs) and expression of collagen matrix via enhancement of Smad7 expression, which were confirmed in LX-2, MES13, and NIH3T3 cells in vitro. In contrast, knockdown of Smad7 in LX-2 cells prevented praziquantel-mediated inhibition of LX-2 cell activation and TGF-β1-mediated collagen type I α1 induction, revealing the critical role of Smad7 in the antifibrotic effect of praziquantel during liver fibrosis. Conclusions and Implications: PZQ exhibited a strong efficacy against liver fibrosis by inhibiting activation of HSCs via Smad7 up-regulation, suggesting potential broad utility in treatment of diseases characterized by liver fibrosis.

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“…This has an obvious bearing on the human situation, where continued stress must be placed on surveillance of high-risk populations for early cholangiocellular tumors as the most effective approach to control. However, further investigation of the interaction between other exogenous factors and praziquantel in bringing about a reversal of fibrotic changes similar to that earlier reported for mice infected with schistosomes 29,30) appears warranted.…”

Section: Discussionmentioning

confidence: 70%

Modulation of Dihydroxy‐di‐n‐propylnitrosamine‐induced Liver Lesion Development in Opisthorchis‐infected Syrian Hamsters by Praziquantel Treatment in Association with Butylated Hydroxyanisole or Dehydroepiandrosterone Administration

Moore

Thamavit

Tiwawech

et al. 1998

Japanese Journal of Cancer Research

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The effects of praziquantel coupled with dehydroepiandrosterone (DHEA) or butylated hydroxyanisole (BHA) administration 16 weeks subsequent to dihydroxy-di-n-propylnitrosamine (DHPN) treatment and infection with Opisthorchis viverrini (OV) on lesion development in the liver of Syrian hamsters were investigated. Animals were given 80 OV metacercariae and then two i.p. injections of DHPN (500 mg/kg body weight) 4 and 5 weeks thereafter. At week 16, groups received praziquantel (250 mg/kg, i.g.) and were placed on normal diet or diet supplemented with BHA (1%) or DHEA (0.6%) until they were killed at week 24. Histopathological assessment revealed that, whereas antihelminthic treatment alone resulted in a clear reduction in hepatocellular lesion development, effects on cholangiocellular lesions were equivocal. BHA and DHEA, in contrast, were both associated with a significant reduction in frequency of cholangiofibrosis and cholangiocellular carcinoma. The former chemical, however, increased the numbers of liver nodules while the hormone brought about a decrease as well as a shift in the phenotype of the lesions. The results thus indicate that although cholangiocellular lesion development may, unlike generation of hepatocellular nodules, be to a certain extent independent of the continued presence of parasite, it can be influenced by exogenous treatments.

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Effect of praziquantel on hepatic fibrosis in experimental Schistosomiasis mansoni

Cited by 18 publications

References 21 publications

Effect of praziquantel prolonged administration on granuloma formation around Schistosoma japonicum eggs in lung of sensitized mice

Effect of praziquantel prolonged administration on granuloma formation around Schistosoma japonicum eggs in lung of sensitized mice

Praziquantel ameliorates CCl₄‐induced liver fibrosis in mice by inhibiting TGF‐β/Smad signalling via up‐regulating Smad7 in hepatic stellate cells

Modulation of Dihydroxy‐di‐n‐propylnitrosamine‐induced Liver Lesion Development in Opisthorchis‐infected Syrian Hamsters by Praziquantel Treatment in Association with Butylated Hydroxyanisole or Dehydroepiandrosterone Administration

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Effect of praziquantel on hepatic fibrosis in experimental Schistosomiasis mansoni

Cited by 18 publications

References 21 publications

Effect of praziquantel prolonged administration on granuloma formation around Schistosoma japonicum eggs in lung of sensitized mice

Effect of praziquantel prolonged administration on granuloma formation around Schistosoma japonicum eggs in lung of sensitized mice

Praziquantel ameliorates CCl4‐induced liver fibrosis in mice by inhibiting TGF‐β/Smad signalling via up‐regulating Smad7 in hepatic stellate cells

Modulation of Dihydroxy‐di‐n‐propylnitrosamine‐induced Liver Lesion Development in Opisthorchis‐infected Syrian Hamsters by Praziquantel Treatment in Association with Butylated Hydroxyanisole or Dehydroepiandrosterone Administration

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Praziquantel ameliorates CCl₄‐induced liver fibrosis in mice by inhibiting TGF‐β/Smad signalling via up‐regulating Smad7 in hepatic stellate cells