Key result
Treatment with the anti-mouse IL-6 receptor antibody MR16-1 completely prevented muscle atrophy in IL-6 transgenic mice, maintaining gastrocnemius muscle weight at normal levels.
Why the study?
Does anti-mouse IL-6 receptor antibody prevent muscle atrophy and modulate proteolytic systems in IL-6 transgenic mice?
Does anti-mouse IL-6 receptor antibody prevent muscle atrophy and modulate proteolytic systems in IL-6 transgenic mice?
Absolute Event Rate: 117.3% vs 91%
p-value: p=<0.05
Anti-IL-6 receptor antibody completely blocks muscle atrophy and normalizes proteolytic system activation in IL-6 transgenic mice, suggesting potential therapeutic utility for muscle wasting in cachexia.
May support IL-6 blockade in cachexia models; leaves open translation to human muscle wasting.
The muscles of IL-6 transgenic mice suffer from atrophy. Experiments were carried out on these transgenic mice to elucidate activation of proteolytic systems in the gastrocnemius muscles and blockage of this activation by treatment with the anti-mouse IL-6 receptor (mIL-6R) antibody. Muscle atrophy observed in 16-wk-old transgenic mice was completely blocked by treatment with the mIL-6R antibody. In association with muscle atrophy, enzymatic activities and mRNA levels of cathepsins (B and L) and mRNA levels of ubiquitins (poly- and mono-ubiquitins) increased, whereas the mRNA level of muscle-specific calpain (calpain 3) decreased. All these changes were completely eliminated by treatment with the mIL-6R antibody. This IL-6 receptor antibody could, therefore, be effective against muscle wasting in sepsis and cancer cachexia, where IL-6 plays an important role.
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Tsujinaka et al. (1996) studied Muscle atrophy (n=14). Anti-mouse IL-6 receptor antibody (MR16-1) vs. PBS was evaluated on Gastrocnemius muscle weight (mg) (p=<0.05). Treatment with the anti-mouse IL-6 receptor antibody MR16-1 completely prevented muscle atrophy in IL-6 transgenic mice, maintaining gastrocnemius muscle weight at normal levels.
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