Objective: To observe the effects of follistatin (FST)on the skeletal muscle wasting of cancer cachexia mice and the expressions of Mstn, LncRNA-MALAT1 and Caspase-3, and to elucidate its associated molecular mechanisms.Methods:Thirty-two BALB/c mices were randomly assigned into:healthy control (HC) group,FST prevention (FP)group,FST treatment (FT)group and cancer cachexia (CC)group.The murine colon adenocarcinoma CT26 cells were inoculated subcutaneously into the mices in FP, FT and CC groups to establish the cancer cachexia models. The body weight, spontaneous activity and tumor growth were daily monitored.The mice in FP and FT groups were administrated with FST intraperitoneally on day 6 and 12 after inoculation.The samples were collected on day 20.The tumor and gastrocnemius weights of the mice were detected. The biochemical metabolism indexes and myofiber cross-sectional area of gastrocnemius tissue were detected.The mRNA expression levels of Mstn,Caspase-3 and LncRNA-MALAT1 were examined by Real-time PCR.The protein expression levels of Mstn and Caspase-3 were measured by Western blotting method. Results:Compared with CC group,the body weights,spontaneous activities,gastrocnemius weights and myofiber cross-sectional areas were increased (P <0.05);the serum levels of glucose,total protein and albumin of the mice in FP and FT groups were increased (P <0.05).The protein and mRNA expression levels of Mstn and Caspase-3 in gastrocnemius of the mice in CC group were significantly higher and the expression level of LncRNA-MALAT1 was significantly lower than those in HC group (P < 0.05).The mRNA and protein expression levels of Mstn and Caspase-3 in FP and FT groups were reduced and the expression level of LncRNA-MALAT1 was increased compared with CC group (P < 0.05).The prevention effect in FP group is better than FT group (P < 0.05). Conclusion:FST may alleviate the muscle wasting of the mice with cancer cachexia by inhibiting the expression of Mstn,thus upregulating the expression of LncRNA-MALAT1 which in turn to suppress the expression of Caspase-3.

[Objective]To investigate the effect of pantoprazole on skeletal muscle wasting in cancer cachexia and the possible mechanism.[Methods]24 male BALB/c mice were randomly divided into control group(NN),cancer cachexia group(CC),pantrop?razole treatment group(PPI). The mice in CC and PPI were inoculated subcutaneously with mouse colon adenocarcinoma C26 cells to establish a model of cancer cachexia. The mice in PPI group were gavaged with 75 mg/kg pantoprazole dissolving in physiological saline,while those in NN and CC group were gavaged with 0.1 mL/10 g physiological saline. The mice were killed 12d after treatment. The weight of gastrocnemius and tumour and the size of tumour were measured. The morphological change of skeletal muscle were evalu?ated by the method of stain with hematoxylin and eosin(H&E). The levels of IL-6 and TNF-αin serum were tested by ELISA. qRT-PCR was used to assess the expression of mRNA of Myod1 and myf5 in skeletal muscle. The protein expressions of MuRF1,MAFBx, Myod1 and myf5 were measured by Western blot.[Results]Compared with CC group ,pantoprazole can increase the weight of mice and gastrocnemius(39.8% and 24.2%,respectively),cross section area(25.4%),levels of mRNA and protein of Myod1 and myf5(P<0.05),while the levels of IL-6 and TNF-αdecreased(30.7%and 18.9%,respectively),as well as the levels of protein ex?pression of MuRF1 and MAFBx(P < 0.05).[Conclusion]Pantoprazole can attenuate the wasting of skeletal muscle,the potential mechanism may be related to the inhibition of inflammatory factors and UPS ,and up-regulation of Myod1 and myf5.