The polyherbal formula described for acute wounds promoted both angiogenesis and fibroblast proliferation and collagen synthesis in a streptozotocin diabetic rat model (Gupta et al., 2008). Dressings impregnated with copper oxide applied to wounds of diabetic mice resulted in the upregulation of the pro-angiogenic factors placental growth factor, hypoxia-inducible factor-1α and VEGF, leading to increased angiogenesis and faster wound closure (Borkow et al., 2010). High-throughput screening of medicinal plants known to be beneficial for blood circulation identified a material named SBD.4a from the plant Angelica sinensis as having angiogenic properties on a par with PDGF-BB (Zhao et al., 2006).
Thymosin beta(4), a small ubiquitous protein containing 43 aa, has structure/function activity via its actin-binding domain and numerous biological affects on cells. Since it is the major actin-sequestering molecule in eukaryotic cells and is found essentially in all cells and body fluids, thymosin beta(4) has the potential for significant roles in tissue development, maintenance, repair, and pathology. Several active sites with unique functions have been identified, including the amino-terminal site containing 4 aa (Ac-SDKP) that generally blocks inflammation and reduces fibrosis. Another active site at the amino terminus contains 15 aa, including Ac-SDKP, and promotes cell survival and blocks apoptosis, while a short sequence containing LKKTETQ, the central actin-binding domain (aa 17-23) plus 1 additional amino acid (Q), promotes angiogenesis, wound healing, and cell migration. Several additional biological activities have been identified but not yet localized in the molecule, including its antimicrobial activity, the induction of various genes (including laminin-5, MMPs, TGF beta, zyxin, terminal deoxynucleotidyl transferase, and angiogenesis-related proteins), and the ability to activate ILK/PINCH/Akt, and other signaling molecules important in both apoptosis and inflammatory pathways. This review details these important physiologically and pathologically active sites and their potential therapeutic uses.
Jump up ^ Low TL, Hu SK, Goldstein AL (February 1981). "Complete amino acid sequence of bovine thymosin beta 4: a thymic hormone that induces terminal deoxynucleotidyl transferase activity in thymocyte populations". Proceedings of the National Academy of Sciences of the United States of America. 78 (2): 1162–6. Bibcode:1981PNAS...78.1162L. doi:10.1073/pnas.78.2.1162. PMC 319967. PMID 6940133.
It should be noted that supplemental 5-HTP can cause an increase in urinary 5-HIAA, which is the major metabolite of serotonin that is excreted in the urine. Increased urinary 5-HIAA is also sometimes a diagonistic marker for carcinoid tumors due to increased conversion of tryptophan to serotonin in these tumors,[62][63] and in this case serum chromogranin A should be measured (as supplemental 5-HTP does not appear to increase chromogranin A).[63]
Obesity. Early research suggests that taking 5-HTP might help reduce appetite, caloric intake, and weight in obese people. Other research suggests that using a specific mouth spray containing 5-HTP and other extracts (5-HTP-Nat Exts, Medestea Biotech S.p.a., Torino, Italy) for 4 weeks increases weight loss by about 41% in overweight postmenopausal women.
For this study, one of us, Ben Trumble, followed Tsimane men as they went hunting for food. Typically, Tsimane men set out alone or with a partner in the early morning and search in the forest for prey such as wild pigs, deer, monkeys, or the rare tapir. Following long looping trails they might be gone for eight or nine hours, traveling about six miles (ten kilometers). Ben collected saliva samples throughout the hunt in order to measure changes in men’s hormone levels.
It has been reported that deficiencies in the amino acid tryptophan (precursor to 5-HTP) are correlated with depression, as evidence by serum tryptophan in depressed persons.[16][17] Decreased levels of tryptophan in the body can come from various means but are most likely caused by a diet lacking in the amino acid as substrate, or by upregulation of enzymes (most notably indoleamine 2,3-dioxygenase(IDO) and tryptophan 2,3-dioxygenase(TDO)) that degrade tryptophan or direct it to paths that are not serotonin synthesis causing a relative deficiency.[18][19] These enzymes can be upregulated in states of chronic inflammation[18][20] and injection of some pro-inflammatory cytokines has been implicated in depression[21] and increasing the kyurenine:tryptophan ratio, which is indicative of IDO activity being increased.[22] The activity of tryptophan hydroxylase can also be further downregulated in cases of Magnesium or vitamin B6 deficiency, stress, or excessive tryptophan levels.[7]
It was also shown recently that delivery of Fgfs by release from peptide nanofibers, a gradual local delivery system, can increase neovascularization and reduce in-farct size in the ischemic rodent heart (Engel et al., 2006). Related to this, zebrafish have a natural ability to synthesize Fgfs after myocardial injury, a signal that appears to recruit Fgf receptor-expressing epicardial-derived cells toward regenerating muscle (Lepilina et al., 2006). Thus, what has been and what will be discovered about zebrafish heart regeneration is quite likely to illuminate possible strategies for enhancing regeneration in the mammalian heart (see Chapter 14.4).
When combined with antidepressants of the MAOI or SSRI class, very high parenteral doses of 5-HTP can cause acute serotonin syndrome in rats.[23][24] It is unclear if such findings have clinical relevance, as most drugs will cause serious adverse events or death in rodents at very high doses. In humans 5-HTP has never been clinically associated with serotonin syndrome, although 5-HTP can precipitate mania when added to an MAOI.[25]
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