ArticleBritish journal of pharmacology2003
The effect of chelerythrine on depolarization-induced force responses in skinned fast skeletal muscle fibres of the rat.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 citing papers in PubMed, 14 citations in OpenAlex.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1 We examined the effect of the protein kinase C (PKC) inhibitor chelerythrine on depolarization-induced force responses (DIFRs) and sarcoplasmic reticulum (SR) function in single, mechanically skinned skeletal muscle fibres of the rat. 2 In this study, the DIFRs in the skinned fibres normally underwent an irreversible loss of excitation-contraction coupling (ECC) after 10-15 responses. Chelerythrine (12 micro M) was shown to restore ECC in these fibres. Restored force responses were similar in peak (control 50.8+/-6.4%, chelerythrine 56.9+/-12.4% of maximum force, P=0.42, n=21), but significantly broadened compared to initial control responses (full-width at half maximum, control; 3.7+/-0.3 s, chelerythrine; 13.3+/-1.1 s, P<0.001). Early exposure to chelerythrine prevented run-down of DIFRs. Chelerythrine also induced spontaneous force responses in some fibres. 3 The PKC inhibitors calphostin C and staurosporine did not restore ECC, and the PKC activator phorbol 12-myristate 13-acetate did not promote loss of ECC in the skinned fibres. 4 Chelerythrine significantly increased SR Ca(2+) loading by 8.4+/-1.7% (P=0.02, n=9) and SR Ca(2+) release by at least 14.1+/-2.7% (P=0.004, n=11) in the skinned fibres. 5 Chelerythrine had no significant effect on maximum force production or the [Ca(2+)] producing half maximal activation of the myofilaments. However, chelerythrine did have a small effect on the slope of the force-Ca(2+) relationship (P=0.02, n=10). 6 Chelerythrine reverses the use-dependent loss of excitation-contraction coupling in skinend skeletal muscle fibres by a PKC independent pathway. Chelerythrine may be an important pharmacological probe for examining the mechanisms of contraction-induced muscle injury.
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