Introduction: Statins are group of drugs used to reduce total and low density lipoprotein (LDL)-cholesterol level and to reduce the morbidity and mortality of cardiovascular diseases. Meanwhile, induced skeletal muscle- specific mitochondrial impairment, oxidative stress and myotoxicity are serious side effects . Vitamin E and ginger extract are well known potent antioxidants. Aim: To study the possible protective effect of ginger extract versus vitamin E against simvastatin- induced skeletal muscle histological and the associated biophysiological changes. Materials and Methods: Forty adult male albino rats were randomly divided into four equal groups (10 rats, each).; Group 1: was the control rats. Group 2: received 0.54 mg/kg/day simvastatin orally for 8 weeks. Group 3: received concomitant treatment of simvastatin and 30 mg/kg/day vitamin E orally for 8 weeks. Group 4 received concomitant treatment of simvastatin and 500mg/kg/day ginger extract orally for 8 weeks. After sacrifice, specimens were taken from the belly of the quadriceps femoris muscles of all animal groups and processed for light and electron microscopy. Biochemical tests and statistical analysis were done. Results: Group 2 showed focal areas of muscle fiber loss, mononuclear cellular infiltration and variable staining density. Ultra structurally, myofibrillar degeneration and accumulation of numerous giant infrequently damaged mitochondria were observed. The skeletal muscle fibers of animals from group 3 and group 4, both were markedly improved. Group 4 revealed obviously normal mitochondria. Conclusion: Administration of simvastatin for 8 weeks induced histological, physiological and biochemical skeletal myotoxic effects. These effects were greatly ameliorated by concomitant administration vitamin E or ginger extract. Ginger extract was more effective.

Introduction: Statins are group of drugs used to reduce total and low density lipoprotein (LDL)-cholesterol level and to reduce the morbidity and mortality of cardiovascular diseases. Meanwhile, induced skeletal muscle- specific mitochondrial impairment, oxidative stress and myotoxicity are serious side effects . Vitamin E and ginger extract are well known potent antioxidants. Aim: To study the possible protective effect of ginger extract versus vitamin E against simvastatin- induced skeletal muscle histological and the associated biophysiological changes. Materials and Methods: Forty adult male albino rats were randomly divided into four equal groups (10 rats, each).; Group 1: was the control rats. Group 2: received 0.54 mg/kg/day simvastatin orally for 8 weeks. Group 3: received concomitant treatment of simvastatin and 30 mg/kg/day vitamin E orally for 8 weeks. Group 4 received concomitant treatment of simvastatin and 500mg/kg/day ginger extract orally for 8 weeks. After sacrifice, specimens were taken from the belly of the quadriceps femoris muscles of all animal groups and processed for light and electron microscopy. Biochemical tests and statistical analysis were done. Results: Group 2 showed focal areas of muscle fiber loss, mononuclear cellular infiltration and variable staining density. Ultra structurally, myofibrillar degeneration and accumulation of numerous giant infrequently damaged mitochondria were observed. The skeletal muscle fibers of animals from group 3 and group 4, both were markedly improved. Group 4 revealed obviously normal mitochondria. Conclusion: Administration of simvastatin for 8 weeks induced histological, physiological and biochemical skeletal myotoxic effects. These effects were greatly ameliorated by concomitant administration vitamin E or ginger extract. Ginger extract was more effective.

Introduction: Statins are group of drugs used to reduce total and low density lipoprotein (LDL)-cholesterol level and to reduce the morbidity and mortality of cardiovascular diseases. Meanwhile, induced skeletal muscle- specific mitochondrial impairment, oxidative stress and myotoxicity are serious side effects . Vitamin E and ginger extract are well known potent antioxidants. Aim: To study the possible protective effect of ginger extract versus vitamin E against simvastatin- induced skeletal muscle histological and the associated biophysiological changes. Materials and Methods: Forty adult male albino rats were randomly divided into four equal groups (10 rats, each).; Group 1: was the control rats. Group 2: received 0.54 mg/kg/day simvastatin orally for 8 weeks. Group 3: received concomitant treatment of simvastatin and 30 mg/kg/day vitamin E orally for 8 weeks. Group 4 received concomitant treatment of simvastatin and 500mg/kg/day ginger extract orally for 8 weeks. After sacrifice, specimens were taken from the belly of the quadriceps femoris muscles of all animal groups and processed for light and electron microscopy. Biochemical tests and statistical analysis were done. Results: Group 2 showed focal areas of muscle fiber loss, mononuclear cellular infiltration and variable staining density. Ultra structurally, myofibrillar degeneration and accumulation of numerous giant infrequently damaged mitochondria were observed. The skeletal muscle fibers of animals from group 3 and group 4, both were markedly improved. Group 4 revealed obviously normal mitochondria. Conclusion: Administration of simvastatin for 8 weeks induced histological, physiological and biochemical skeletal myotoxic effects. These effects were greatly ameliorated by concomitant administration vitamin E or ginger extract. Ginger extract was more effective.

Introduction: Statins are group of drugs used to reduce total and low density lipoprotein (LDL)-cholesterol level and to reduce the morbidity and mortality of cardiovascular diseases. Meanwhile, induced skeletal muscle- specific mitochondrial impairment, oxidative stress and myotoxicity are serious side effects . Vitamin E and ginger extract are well known potent antioxidants. Aim: To study the possible protective effect of ginger extract versus vitamin E against simvastatin- induced skeletal muscle histological and the associated biophysiological changes. Materials and Methods: Forty adult male albino rats were randomly divided into four equal groups (10 rats, each).; Group 1: was the control rats. Group 2: received 0.54 mg/kg/day simvastatin orally for 8 weeks. Group 3: received concomitant treatment of simvastatin and 30 mg/kg/day vitamin E orally for 8 weeks. Group 4 received concomitant treatment of simvastatin and 500mg/kg/day ginger extract orally for 8 weeks. After sacrifice, specimens were taken from the belly of the quadriceps femoris muscles of all animal groups and processed for light and electron microscopy. Biochemical tests and statistical analysis were done. Results: Group 2 showed focal areas of muscle fiber loss, mononuclear cellular infiltration and variable staining density. Ultra structurally, myofibrillar degeneration and accumulation of numerous giant infrequently damaged mitochondria were observed. The skeletal muscle fibers of animals from group 3 and group 4, both were markedly improved. Group 4 revealed obviously normal mitochondria. Conclusion: Administration of simvastatin for 8 weeks induced histological, physiological and biochemical skeletal myotoxic effects. These effects were greatly ameliorated by concomitant administration vitamin E or ginger extract. Ginger extract was more effective.

Abstract Ageing is associated with decreased lung function and an increased incidence of lung infections. Several studies have suggested that long‐term calorie restriction (CR) promotes health and longevity and results in the reduced risk of several diseases. The effect of CR is thought to be through improving the function of tissue stem cells. Stem cell function is known to decline with ageing. In this study, we examined the effects of ageing on lung epithelial and stem cells and the effect of CR on young and old lungs. We found that ageing results in a decrease in tracheal basal stem cells. CR induced an increase in basal stem cells in both young and old mice. In addition, ageing induced lung inflammation, and CR tended to reduce baseline lung inflammatory cell infiltration in young mice and significantly reduced ageing‐induced lung inflammation. Furthermore, ageing reduced the number and function of mitochondria in lung and increased the level of mitochondrial reactive oxygen species. CR increased the number and function of mitochondria both in young and old mice. Moreover, ageing reduced lung stem cell colony‐forming efficiency (CFE), and CR increased the CFE in both young and old mice. Finally, CR improved epithelial cell survival in injured lungs of young mice. In conclusion, ageing causes several structural and functional changes/impairments in lung epithelial cells. CR induces several potentially beneficial changes in lung epithelial cells, even when it is initiated at an older age, including reversal of some ageing‐induced changes.

Introduction: Schistosomiasis is one of the most prevalent parasitic infections in developing countries. Although chemotherapy is one of the main strategies in controlling the disease, it is less effective in reversal of schistosome-induced pathology especially in the chronic and advanced stages of schistosomiasis. New strategies and prospective therapeutic agents with antifibrotic effects are needed. Eugenol has a wide anti-inflammatory effect. In the present study, we investigated the possible antischistosomal effect of eugenol on Schistosoma mansoni. Materials and methods: The murine model of S. mansoni was established in three groups of adult male Balb-c mice; group I (infected non-treated group) and groups II and III (infected groups) treated orally with eugenol and praziquantel (PZQ), respectively. The expression of the sensitive immunohistochemical marker α-smooth muscle actin (α-SMA) in schistosome-infected tissues was determined. In addition, parasitological, biochemical, and histological parameters that reflect disease severity and morbidity were examined. Results: Eugenol treatment showed significant reduction in total worm burden by 19.2%; however, the oogram pattern showed no marked difference compared to that of the PZQ group. Yet, eugenol significantly reduced the serum levels of hepatic enzymes: aspartate aminotransferase and alanine aminotransferase. Histopathological examination revealed a significant reduction in both numbers and diameters of hepatic granulomata, which was consistent with reduction in collagen fiber deposition. Additionally, the antifibrotic effect of eugenol was validated by its considerable reduction in the expression of the sensitive marker α-SMA in both eugenol- and PZQ-treated groups. Conclusion: Although eugenol could not totally eradicate adults of S. mansoni, the significant amelioration of liver enzymes and hepatic fibrosis potentiate eugenol’s role as a promising antifibrotic and a complementary antischistosomal agent.

Introduction: Schistosomiasis is one of the most prevalent parasitic infections in developing countries. Although chemotherapy is one of the main strategies in controlling the disease, it is less effective in reversal of schistosome-induced pathology especially in the chronic and advanced stages of schistosomiasis. New strategies and prospective therapeutic agents with antifibrotic effects are needed. Eugenol has a wide anti-inflammatory effect. In the present study, we investigated the possible antischistosomal effect of eugenol on Schistosoma mansoni. Materials and methods: The murine model of S. mansoni was established in three groups of adult male Balb-c mice; group I (infected non-treated group) and groups II and III (infected groups) treated orally with eugenol and praziquantel (PZQ), respectively. The expression of the sensitive immunohistochemical marker α-smooth muscle actin (α-SMA) in schistosome-infected tissues was determined. In addition, parasitological, biochemical, and histological parameters that reflect disease severity and morbidity were examined. Results: Eugenol treatment showed significant reduction in total worm burden by 19.2%; however, the oogram pattern showed no marked difference compared to that of the PZQ group. Yet, eugenol significantly reduced the serum levels of hepatic enzymes: aspartate aminotransferase and alanine aminotransferase. Histopathological examination revealed a significant reduction in both numbers and diameters of hepatic granulomata, which was consistent with reduction in collagen fiber deposition. Additionally, the antifibrotic effect of eugenol was validated by its considerable reduction in the expression of the sensitive marker α-SMA in both eugenol- and PZQ-treated groups. Conclusion: Although eugenol could not totally eradicate adults of S. mansoni, the significant amelioration of liver enzymes and hepatic fibrosis potentiate eugenol’s role as a promising antifibrotic and a complementary antischistosomal agent.

Introduction: Schistosomiasis is one of the most prevalent parasitic infections in developing countries. Although chemotherapy is one of the main strategies in controlling the disease, it is less effective in reversal of schistosome-induced pathology especially in the chronic and advanced stages of schistosomiasis. New strategies and prospective therapeutic agents with antifibrotic effects are needed. Eugenol has a wide anti-inflammatory effect. In the present study, we investigated the possible antischistosomal effect of eugenol on Schistosoma mansoni. Materials and methods: The murine model of S. mansoni was established in three groups of adult male Balb-c mice; group I (infected non-treated group) and groups II and III (infected groups) treated orally with eugenol and praziquantel (PZQ), respectively. The expression of the sensitive immunohistochemical marker α-smooth muscle actin (α-SMA) in schistosome-infected tissues was determined. In addition, parasitological, biochemical, and histological parameters that reflect disease severity and morbidity were examined. Results: Eugenol treatment showed significant reduction in total worm burden by 19.2%; however, the oogram pattern showed no marked difference compared to that of the PZQ group. Yet, eugenol significantly reduced the serum levels of hepatic enzymes: aspartate aminotransferase and alanine aminotransferase. Histopathological examination revealed a significant reduction in both numbers and diameters of hepatic granulomata, which was consistent with reduction in collagen fiber deposition. Additionally, the antifibrotic effect of eugenol was validated by its considerable reduction in the expression of the sensitive marker α-SMA in both eugenol- and PZQ-treated groups. Conclusion: Although eugenol could not totally eradicate adults of S. mansoni, the significant amelioration of liver enzymes and hepatic fibrosis potentiate eugenol’s role as a promising antifibrotic and a complementary antischistosomal agent.

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