Study On The Mechanism Of Linolenic Acid To Improve Sarcopenia Of C.elegans

Linolenic acid is an essential fatty acid that cannot be synthesized by the human body.It plays an important role in many physiological activities,such as anti-inflammatory and antioxidant.Sarcopenia,a metabolic syndrome of age-related loss of muscle mass and strength,is a common but overlooked and undertreated syndrome of aging.Sarcopenia seriously affects the quality of life of the elderly.Studies have shown that EPA and DHA have a potential effect on the improvement of sarcopenia,whereas the effect of linolenic acid,an essential n-3 fatty acid,on sarcopenia has been poorly reported.Therefore,in order to explore whether linolenic acid can ameliorate sarcopenia and explain its mechanism,the following work was completed in this study:First,the effects of aging on muscle were simulated using a Caenorhabditis elegans(C.elegans)model.The results showed that with aging,the muscle protein content of C.elegans decreased gradually,the exercise ability was deficient,and the sarcomere structure was damaged and the body atrophied.When linolenic acid concentration reached 50 μg/m L,muscle protein content of C.elegans increased by 19.2% compared with the control group(p<0.05),the movement speed increased by 22 times/min(p<0.05),and the sarcomere structure damage and body atrophy of C.elegans were reversed.Subsequently,specific genes were selected to modify C.elegans model,and the mechanism of linolenic acid to improve C.elegans sarcopenia was further studied in terms of mitochondrial function and oxidative stress.The results showed that the application of linolenic acid to C.elegans could alleviate the mitochondrial damage caused by aging.In addition,compared with the blank control group,the activity of mitochondrial electron transport chain complex was increased in the linolenic acid intervention group,and the level of ATP in mitochondria was increased by 1.2 times(p<0.05),mitochondrial membrane potential increased by 2.2 times(p<0.05),suggesting that linolenic acid has a role in repairing mitochondrial dysfunction.The effect of linolenic acid on mitochondria autophagy gene pink-1 in C.elegans was further investigated.The results showed that linolenic acid can promote mitochondrial autophagy by increasing the expression level of pink-1 to repair mitochondrial dysfunction.In terms of oxidative stress,linolenic acid significantly reduced the accumulation of reactive oxygen species(ROS)in C.elegans and increased the total antioxidant capacity in C.elegans.Linolenic acid increases the expression of the DAF-16/FOXO transcription factor and the downstream sod-3 gene involved in oxidation resistance in C.elegans cells.The daf-16 gene mutant C.elegans has been used to demonstrate that linolenic acid regulates ROS content through the DAF-16 signaling pathway.Finally,in order to develop food formulations that can be used to improve sarcopenia,this study combined linolenic acid with other nutrients to investigate whether it has a synergistic effect on improving sarcopenia.The results showed that when linolenic acid was combined with vitamin D at the concentration of 50 μg/m L and 40 μg/m L,the synergistic effect was significantly better than that of linolenic acid alone(p<0.05).When linolenic acid was combined with coenzyme Q,there was no significant change in its effect on sarcopenia(p>0.05).In summary,this study systematically analyzed the intervention effect of linolenic acid on senility induced sarcopenia by using C.elegans model,and found that linolenic acid can promote autophagy of mitochondria by increasing the expression level of mitochondrial autophagy gene pink-1,so as to repair mitochondrial function.In addition,linolenic acid can improve muscle attenuation by increasing DAF-16/FOXO transcription factor expression,reducing ROS accumulation and countering oxidative stress response.Through the implementation of this work,it provides a certain theoretical reference for the prevention and improvement of senility induced sarcopenia by linolenic acid.