Cyclophosphamide(CP) is a widely used anti-cancer agent; however, it can also induce serious male infertility. There are currently no effective drugs to alleviate this side-effect. L-Carnitine has been used to treat m...Cyclophosphamide(CP) is a widely used anti-cancer agent; however, it can also induce serious male infertility. There are currently no effective drugs to alleviate this side-effect. L-Carnitine has been used to treat male infertility, but whether it can be used to protect against CP-induced male infertility is still unclear. This study aims to explore the effect and mechanism of L-carnitine in male infertility induced by CP. CP was used to establish an animal model. After three weeks of treatment, rats were sacrificed and testis and serum were harvested for further evaluation. Testosterone and estrogen levels were measured by enzyme-linked immunosorbent assay(ELISA). Testicular injury was examined by hematoxylin and eosin(H & E) staining, and germ-cell apoptosis was evaluated by terminal deoxynucleotidyl transferase dU TP nick end labeling(TUNEL). The expression of LC3 and Beclin-1 was examined by immunohistochemistry, Western blot, and real-time polymerase chain reaction(PCR), respectively. Compared with the CP group, L-carnitine significantly increases sperm motility, viability, and testosterone level(P<0.05). Western blot and real-time PCR results showed that L-carnitine treatment can significantly up-regulate the LC3-II and Beclin-1 expression in the CP+L-carnitine group when compared with the control group(P<0.05). In addition, TUNEL-positive cells were also more numerous in the CP group; however, L-carnitine can effectively retard cell apoptosis in the CP+ L-carnitine group. In conclusion, L-carnitine contributes to the inhibition of cell apoptosis and the modulation of autophagy in protecting CP-induced testicular injury. These results suggest the applicability of L-carnitine in the treatment of male infertility.展开更多
Objective： Statins＇ therapy in osteoporosis can aggravate muscle damage. This study was designed to assess which agent, L-carnitine or coenzyme Q10, could enhance the anti-osteoporotic effect of atorvastatin while a...Objective： Statins＇ therapy in osteoporosis can aggravate muscle damage. This study was designed to assess which agent, L-carnitine or coenzyme Q10, could enhance the anti-osteoporotic effect of atorvastatin while antagonizing myopathy in ovariectomized rats. Methods： Forty-eight female Sprague Dawley rats were used; forty rats were ovariectomized while eight were sham-operated. Eight weeks post-ovariectomy, rats were divided into ovariectomized-untreated group and four ovadectomized-treated groups （n=8） which received by gavage （mg/（kg.d）, for 8 weeks） 17^-estradiol （0.1）, atorvastatin （50）, atorvastatin （50）＋L-carnitine （100）, or atorvastatin （50）＋coenzyme Q10 （20）. At the end of therapy, bone mineral density （BMD）, bone mineral content （BMC）, and serum levels of bone metabolic markers （BMMs） and creatine kinase （CK） were measured. Femurs were used for studying the breaking strength and histopathological changes. Results： Treatment with atorvastatin＋L-carnitine restored BMD, BMC, and bone strength to near normal levels. Estrogen therapy restored BMD and BMC to near normal levels, but failed to increase bone strength. Although atorvastatin and atorvastatin＋coenzyme Q10 improved BMD, BMC, and bone strength, they failed to restore levels to normal. All treatments decreased BMMs and improved histopathological changes maximally with atorvastatin＋L-carnitine which restored levels to near normal. Atorvastatin aggravated the ovariectomy-induced increase in CK level while estrogen, atorvastatin＋L-carnitine, and atorvastatin＋coenzyme Q10 decreased its level mainly with atorvastatin＋L-camitine which restored the level to near normal. Conclusions： Co- administration of L-carnitine, but not coenzyme Q10, enhances the anti-osteoporotic effect of atorvastatin while an- tagonizing myopathy in ovariectomized rats. This could be valuable in treatment of osteoporotic patients. However, further confirmatory studies are needed.展开更多
基金supported by the National Natural Sciene Foundation of China(No.81402814)
文摘Cyclophosphamide(CP) is a widely used anti-cancer agent; however, it can also induce serious male infertility. There are currently no effective drugs to alleviate this side-effect. L-Carnitine has been used to treat male infertility, but whether it can be used to protect against CP-induced male infertility is still unclear. This study aims to explore the effect and mechanism of L-carnitine in male infertility induced by CP. CP was used to establish an animal model. After three weeks of treatment, rats were sacrificed and testis and serum were harvested for further evaluation. Testosterone and estrogen levels were measured by enzyme-linked immunosorbent assay(ELISA). Testicular injury was examined by hematoxylin and eosin(H & E) staining, and germ-cell apoptosis was evaluated by terminal deoxynucleotidyl transferase dU TP nick end labeling(TUNEL). The expression of LC3 and Beclin-1 was examined by immunohistochemistry, Western blot, and real-time polymerase chain reaction(PCR), respectively. Compared with the CP group, L-carnitine significantly increases sperm motility, viability, and testosterone level(P<0.05). Western blot and real-time PCR results showed that L-carnitine treatment can significantly up-regulate the LC3-II and Beclin-1 expression in the CP+L-carnitine group when compared with the control group(P<0.05). In addition, TUNEL-positive cells were also more numerous in the CP group; however, L-carnitine can effectively retard cell apoptosis in the CP+ L-carnitine group. In conclusion, L-carnitine contributes to the inhibition of cell apoptosis and the modulation of autophagy in protecting CP-induced testicular injury. These results suggest the applicability of L-carnitine in the treatment of male infertility.
文摘Objective： Statins＇ therapy in osteoporosis can aggravate muscle damage. This study was designed to assess which agent, L-carnitine or coenzyme Q10, could enhance the anti-osteoporotic effect of atorvastatin while antagonizing myopathy in ovariectomized rats. Methods： Forty-eight female Sprague Dawley rats were used; forty rats were ovariectomized while eight were sham-operated. Eight weeks post-ovariectomy, rats were divided into ovariectomized-untreated group and four ovadectomized-treated groups （n=8） which received by gavage （mg/（kg.d）, for 8 weeks） 17^-estradiol （0.1）, atorvastatin （50）, atorvastatin （50）＋L-carnitine （100）, or atorvastatin （50）＋coenzyme Q10 （20）. At the end of therapy, bone mineral density （BMD）, bone mineral content （BMC）, and serum levels of bone metabolic markers （BMMs） and creatine kinase （CK） were measured. Femurs were used for studying the breaking strength and histopathological changes. Results： Treatment with atorvastatin＋L-carnitine restored BMD, BMC, and bone strength to near normal levels. Estrogen therapy restored BMD and BMC to near normal levels, but failed to increase bone strength. Although atorvastatin and atorvastatin＋coenzyme Q10 improved BMD, BMC, and bone strength, they failed to restore levels to normal. All treatments decreased BMMs and improved histopathological changes maximally with atorvastatin＋L-carnitine which restored levels to near normal. Atorvastatin aggravated the ovariectomy-induced increase in CK level while estrogen, atorvastatin＋L-carnitine, and atorvastatin＋coenzyme Q10 decreased its level mainly with atorvastatin＋L-camitine which restored the level to near normal. Conclusions： Co- administration of L-carnitine, but not coenzyme Q10, enhances the anti-osteoporotic effect of atorvastatin while an- tagonizing myopathy in ovariectomized rats. This could be valuable in treatment of osteoporotic patients. However, further confirmatory studies are needed.
