Mitochondrial dysfunction: roles in skeletal muscle atrophy.

Mitochondria play important roles in maintaining cellular homeostasis and skeletal muscle health, and damage to mitochondria can lead to a series of pathophysiological changes. Mitochondrial dysfunction can lead to skeletal muscle atrophy, and its molecular mechanism leading to skeletal muscle atrophy is complex. Understanding the pathogenesis of mitochondrial dysfunction is useful for the prevention and treatment of skeletal muscle atrophy, and finding drugs and methods to target and modulate mitochondrial function are urgent tasks in the prevention and treatment of skeletal muscle atrophy. In this review, we first discussed the roles of normal mitochondria in skeletal muscle. Importantly, we described the effect of mitochondrial dysfunction on skeletal muscle atrophy and the molecular mechanisms involved. Furthermore, the regulatory roles of different signaling pathways (AMPK-SIRT1-PGC-1α, IGF-1-PI3K-Akt-mTOR, FoxOs, JAK-STAT3, TGF-ß-Smad2/3 and NF-κB pathways, etc.) and the roles of mitochondrial factors were investigated in mitochondrial dysfunction. Next, we analyzed the manifestations of mitochondrial dysfunction in muscle atrophy caused by different diseases. Finally, we summarized the preventive and therapeutic effects of targeted regulation of mitochondrial function on skeletal muscle atrophy, including drug therapy, exercise and diet, gene therapy, stem cell therapy and physical therapy. This review is of great significance for the holistic understanding of the important role of mitochondria in skeletal muscle, which is helpful for researchers to further understanding the molecular regulatory mechanism of skeletal muscle atrophy, and has an important inspiring role for the development of therapeutic strategies for muscle atrophy targeting mitochondria in the future.

Marketing Archive Management of Drama Intangible Cultural Heritage Based on Particle Swarm Algorithm.

Each Chinese region has its own ancient opera, which is a treasure of folk culture and a living fossil for studying the historical origins of a local culture. It has significant academic value and historical significance at the national and local levels, whether from the perspective of promoting and disseminating national culture or from the perspective of protecting the world's intangible cultural heritage. Based on this practical significance, this paper conducts a study using the particle swarm algorithm to manage the marketing archives of drama intangible cultural heritage. The article employs the PSO algorithm to test the particle swarm optimization algorithm's convergence and conditions. The effectiveness of the algorithm is analysed in the Sphere function, Rosenbrock function, Griewanks function, and Rastrigin noncont function, and then the algorithm is compared, including the calculation speed comparison between the algorithm in this paper and the three optimal fitness functions. The experimental results show that the PSO algorithm has the highest four items in the statistics of the Schwefel function experimental results. About 45.0379 is the best value and 70.5878 is the maximum precision. The optimal average value is 6.1524, while the average value is 56.15245. In comparison to the QPSO and PSO algorithms, the algorithm in this paper has a faster convergence speed and better search accuracy. The topic of the intersection of the disciplines of drama, intangible cultural heritage marketing, and archive management using the particle swarm algorithm is well-developed.

Shikonin attenuates lipopolysaccharide-induced acute lung injury in mice.

BACKGROUND: Shikonin, a natural naphthoquinone pigment extracted from the root of Lithospermum erythrorhizon, has shown a variety of pharmacologic properties including anti-inflammatory effect. In the present study, we analyzed the role of shikonin in acute lung injury induced by lipopolysaccharide (LPS) in mice. MATERIALS AND METHODS: Sixty male BALB/C mice were randomly allocated into six groups (n = 10, each): control group, shikonin group (50 mg/kg), LPS group, and three different doses (12.5, 25, and 50 mg/kg) for shikonin-treated groups. Shikonin or vehicle was given with an intragastric administration 1 h before an intratracheal instillation of LPS (5 mg/kg). The severity of pulmonary injury was evaluated 6 h after LPS challenge. RESULTS: Shikonin pretreatment significantly attenuated LPS-induced pulmonary histopathologic changes, alveolar hemorrhage, and neutrophil infiltration. The lung wet-to-dry weight ratios, as the index of pulmonary edema, were markedly decreased by shikonin pretreatment. Moreover, shikonin decreased the productions of the proinflammatory cytokines including tumor necrosis factor alpha and interleukin 1ß and the concentration of total proteins in the bronchoalveolar lavage fluid. Shikonin pretreatment also reduced the concentrations of myeloperoxidase and nitric oxide in lung tissues. In addition, shikonin pretreatment significantly suppressed LPS-induced activation of cyclooxygenase 2 and inducible nitric oxide synthase and the nuclear factor κB DNA-binding activity in lung tissues. CONCLUSIONS: This study indicates that shikonin may have a protective effect against LPS-induced acute lung injury, and the potential mechanism of this action may attribute partly to the inhibition of inducible nitric oxide synthase and cyclooxygenase 2 expression by downregulating nuclear factor κB activation.