MingHenry said:
I've just started my 3d week of SS31 today. I stopped using lipo-c with NAD+ (Pegasus from Kimera Chems) for a few weeks before starting ss31 because I wanted to feel whatever there might be to feel with ss31, without external energy. And I'm very glad that I did. I plan on doing the three stages of this protocol - ss31/mots-c/Nad+ - in that order - and either for 8 weeks each or 12 weeks each. Though I have no scientific data to point to, I think that using ss31 not only cleans the mitochondria (whether you "feel" anything or not, it's working behind the scenes), but I think it also primes the cells for all the other peps you might research afterwards. I am doing ss31 daily, started low at 1mg, and have moved up to 3mg. I like how I feel - good clean energy and though I'm usually very focused, I do feel like my focus has become even more intense! Though the typical ss31 protocol seems to be 4mg off the bat, daily, running for 21 or 28 days or 1 month or 2 months or more, I wanted to move up slowly and I'm glad I am doing that too - so I started at 1mg, moved to 1.5mg, 2mg, 2.5mg, and now at 3mg over fourteen days. I think I'll stay at 3mg for the whole of this week and then reassess, staying at 3mg or moving up to 3.5mg. Once I decide whether to run ss31 for 8 or 12 weeks, I will add in mots-c about 3 weeks before I finish ss-31. The typical protocol for mots seems to be 5mg 3x a week, but I intend to start low there too, at 1mg again, to see how I react. I'll run mots-c, and increase dosing as feels right to me, drop the ss-31, continue the mots- and either at 8 weeks or 12, I'll introduce the NAD+, and again, I'll start low, not at 25mg with a fast titration schedule up, but at 10mg 3x a week, and move up slowly as I see fit. I can see keeping ss31 as a regular part of my pep protocols.
More info on ss31 and what you may have experienced (generated with scite.ai):
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Based on the references provided, the key points about the use of SS31 peptide are:
- SS31 is a mitochondria-targeted antioxidant peptide that can inhibit apoptosis and oxidative stress by maintaining mitochondrial structure and function (1, 2, 3, 4). It has been shown to protect against various conditions involving mitochondrial dysfunction, such as sepsis-induced muscle weakness (2), atrial fibrillation (5), high glucose-induced neuronal damage (3), and tert-butylhydroperoxide-induced oxidative damage in retinal cells (4).
- SS31 has also been used in combination with other drugs or nanoparticles to enhance their therapeutic effects, such as in the treatment of myocardial ischemia-reperfusion injury (1, 6), Alzheimer's disease (7), and abdominal aortic aneurysm (8).
- The protective effects of SS31 have been attributed to its ability to reduce mitochondrial ROS production, stabilize mitochondrial membrane potential, and modulate signaling pathways like the p38 MAPK pathway (9, 10).
In summary, the references indicate that SS31 is a promising mitochondria-targeted antioxidant with a wide range of therapeutic applications, particularly in conditions involving mitochondrial dysfunction and oxidative stress.
References:
1. Zhang, Z., Chen, Z., Yang, L., Zhang, J., Li, Y., Li, C., … & Xiao, W. (2022). Platelet membrane–encapsulated msns loaded with ss31 peptide alleviate myocardial ischemia-reperfusion injury. *Journal of Functional Biomaterials, 13*(4), 181. https://doi.org/10.3390/jfb13040181
2. Supinski, G., Wang, L., Schroder, E., & Callahan, L. (2020). Ss31, a mitochondrially targeted antioxidant, prevents sepsis-induced reductions in diaphragm strength and endurance. *Journal of Applied Physiology, 128*(3), 463-472. https://doi.org/10.1152/japplphysiol.00240.2019
3. Cao, M., Jiang, J., Du, Y., & Yan, P. (2012). Mitochondria-targeted antioxidant attenuates high glucose-induced p38 mapk pathway activation in human neuroblastoma cells. *Molecular Medicine Reports, 5*(4), 929-934. https://doi.org/10.3892/mmr.2012.746
4. Ma, W., Zhu, X., Ding, X., Li, T., Hu, Y., Hu, X., … & Tang, S. (2015). Protective effects of ss31 on t-bhp induced oxidative damage in 661w cells. *Molecular Medicine Reports, 12*(4), 5026-5034. https://doi.org/10.3892/mmr.2015.4055
5. Wiersma, M., Marion, D., Wüst, R., Houtkooper, R., Zhang, D., Groot, N., … & Brundel, B. (2019). Mitochondrial dysfunction underlies cardiomyocyte remodeling in experimental and clinical atrial fibrillation. *Cells, 8*(10), 1202. https://doi.org/10.3390/cells8101202
6. Li, F., Liu, D., Liu, M., Q, J., Zhang, B., Mei, Q., … & Zhou, S. (2022). Tregs biomimetic nanoparticle to reprogram inflammatory and redox microenvironment in infarct tissue to treat myocardial ischemia reperfusion injury in mice. *Journal of Nanobiotechnology, 20*(1). https://doi.org/10.1186/s12951-022-01445-2
7. Qian, K., Bao, X., Li, Y., Wang, P., Guo, Q., Yang, P., … & Zhang, Q. (2022). Cholinergic neuron targeting nanosystem delivering hybrid peptide for combinatorial mitochondrial therapy in Alzheimer’s disease. *ACS Nano, 16*(7), 11455-11472. https://doi.org/10.1021/acsnano.2c05795
8. Navas‐Madroñal, M., Almendra‐Pegueros, R., Puertas-Umbert, L., Jiménez‐Altayó, F., Julve, J., Pérez, B., … & Galán, M. (2023). Targeting mitochondrial stress with szeto‐schiller 31 prevents experimental abdominal aortic aneurysm: crosstalk with endoplasmic reticulum stress. *British Journal of Pharmacology, 180*(17), 2230-2249. https://doi.org/10.1111/bph.16077
9. Sakellariou, G., Pearson, T., Lightfoot, A., Nye, G., Wells, N., Giakoumaki, I., … & McArdle, A. (2016). Mitochondrial ros regulate oxidative damage and mitophagy but not age-related muscle fiber atrophy. *Scientific Reports, 6*(1). https://doi.org/10.1038/srep33944
10. Zhang, L., Feng, M., Wang, X., Zhang, H., Ding, J., Cheng, Z., … & Qian, L. (2021). Peptide szeto‑schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 mapk signaling pathway. *International Journal of Molecular Medicine, 47*(4). https://doi.org/10.3892/ijmm.2021.4896