Substance P, Free Acid
目录号 : GC37699
Substance P, Free Acid 是 substance P 的类似物，但是不具有 substance P 的生物活性。
Cas No.:71977-09-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Substance P, Free Acid is a native substance P analog, but shows no biological activity of substance P.
[1]. Patel AB, et al. Substance P (free acid) adopts different conformation than native peptide in DMSO, water and DPPC bilayers. J Biomol Struct Dyn. 2001 Aug;19(1):129-38.
| Cas No. | 71977-09-8 | SDF | |
| 分子式 | C63H97N17O14S | 分子量 | 1348.61 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.7415 mL | 3.7075 mL | 7.415 mL |
| 5 mM | 0.1483 mL | 0.7415 mL | 1.483 mL |
| 10 mM | 0.0742 mL | 0.3708 mL | 0.7415 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Molecular mechanisms of depression: perspectives on new treatment strategies
Cell Physiol Biochem 2013;31(6):761-77.PMID:23735822DOI:10.1159/000350094.
Depression is a multicausal disorder and has been associated with the risk to develop cancer, dementia, diabetes, epilepsy and stroke. As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. As a cardiovascular disease a close relationship exists between depression and blood pressure, heart rate, norepinephrine, sympathetic tone, vascular resistance, blood viscosity, plasma volume, intima thickness and atherosclerosis. Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. As an endocrinological and stress disorder depression has been connected with the concentration of free T4, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, Substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. Nutritional factors might influence depression risk, i.e. the consumption of folate, omega-3 fatty acids, monounsaturated fatty acids, olive oil, fish, fruits, vegetables, nuts, legumes, vitamin B6 and vitamin B12. The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. In this context, a fast neuroprotective and antidepressant effect has also been observed by ketamine, which acts via the glutamatergic system. Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. Alternative, causative or also easy available treatment strategies beyond serotonin and noradrenaline reuptake inhibition might be a major topic of future psychiatric care. In this review, an attempt is made to overview concepts of the disease and search for perspectives on antidepressant treatment strategies beyond approved medications.
Salivary Substance P, 5-hydroxytryptamine, and gamma-aminobutyric acid levels in migraine and tension-type headache
Headache 1996 Feb;36(2):100-04.PMID:8742682DOI:10.1046/j.1526-4610.1996.3602101.x.
Substance P, 5-hydroxytryptamine, and gamma-aminobutyric acid levels in saliva were measured in 55 patients with migraine during headache attacks (15 men and 40 women, average age 37.6 years), 36 patients with migraine in interictal periods (8 men and 28 women, average age 43.9 years), 48 patients with tension-type headache during headache attacks (18 men and 30 women, average age 47.3 years), and 25 patients with tension-type headache in interictal periods (10 men and 15 women, average age 48.6 years). Forty-three normal healthy volunteers composed the control group (17 men and 26 women, average age 32.7 years). Substance P levels in saliva were determined using competitive enzyme-linked immunosorbent assay, and were 26.9 +/- 45.1 pmol/mL in the patients with migraine during headache attacks, 30.0 +/- 59.7 pmol/mL in the patients with migraine in interictal periods, 243.5 +/- 1137 pmol/mL in the patients with tension-type headache during headache attacks, 101.3 +/- 364 pmol/mL in the patients with tension-type headache in interictal periods, and 21.2 +/- 17.4 pmol/mL in the healthy controls. 5-hydroxytryptamine levels in saliva were determined using reversed-phase high-performance liquid chromatography with electrochemical detection, and were 895 +/- 1075 ng/mL in the patients with migraine during headache attacks, 758 +/- 1375 ng/mL in the patients with migraine in interictal periods, 1646 +/- 1945 ng/mL in the patients with tension-type headache during active headache periods, 1167 +/- 1495 ng/mL in the patients with tension-type in headache-free periods, and 450 +/- 405 ng/mL in the healthy controls. Gamma-aminobutyric acid levels in saliva were determined using high-performance liquid chromatography with precolumn ortho-phthalaldehyde fluorescence detection. Gamma-aminobutyric acid levels in saliva were 36.8 +/- 49.8 pmol/mL in the patients with migraine during headache attacks, 17.9 +/- 25.2 pmol/mL in the patients with migraine in interictal periods, 16.0 +/- 18.3 pmol/mL in the patients with tension-type headache during active headache periods, 14.1 +/- 6.8 pmol/mL in the patients with tension-type headache in headache-free periods, and 21.6 +/- 22.7 pmol/mL in the healthy controls. The salivary Substance P and 5-hydroxytryptamine levels in the patients with tension-type headache during active headache periods were significantly higher than those in healthy controls. In contrast, we found no significant differences between the salivary gamma-aminobutyric acid levels in the patients with tension-type headache and healthy controls. The high levels of salivary Substance P and 5-hydroxytryptamine in tension-type headache patients during headache periods might reflect release of Substance P from the pain sensory system. Saliva could represent a fluid particularly suitable to the study of neuropeptide release under specific conditions such as migraine and tension-type headache.
Effects of Substance P and substance K on the growth of cultured keratinocytes
J Invest Dermatol 1988 Mar;90(3):399-401.PMID:2450147DOI:10.1111/1523-1747.ep12456487.
The effects of Substance P and substance K, which are coexpressed in the same mRNA as a beta-preprotachykinin in peripheral tissues and released in the inflammatory lesion of the skin, were examined on epidermal proliferation using spontaneously transformed mouse epidermal cell line (Pam 212 cells). Substance P stimulated the synthesis of DNA of Pam 212 cells in the medium containing 2%-10% fetal calf serum (FCS). Stimulation of DNA synthesis was dose dependent if the cells were cultured in the medium containing 2% FCS (quiescent condition). This effect was inhibited by spantide. In a serum-free medium, Substance P had no effect on keratinocyte proliferation. In contrast, substance K, which shares a common amino acid sequence with Substance P on its C-terminal, did not affect DNA synthesis of Pam 212 cells in either medium condition. Substance P released in inflammation may stimulate epidermal proliferation.
Generation of neurons and astrocytes from isolated cells of the adult mammalian central nervous system
Science 1992 Mar 27;255(5052):1707-10.PMID:1553558DOI:10.1126/science.1553558.
Neurogenesis in the mammalian central nervous system is believed to end in the period just after birth; in the mouse striatum no new neurons are produced after the first few days after birth. In this study, cells isolated from the striatum of the adult mouse brain were induced to proliferate in vitro by epidermal growth factor. The proliferating cells initially expressed nestin, an intermediate filament found in neuroepithelial stem cells, and subsequently developed the morphology and antigenic properties of neurons and astrocytes. Newly generated cells with neuronal morphology were immunoreactive for gamma-aminobutyric acid and Substance P, two neurotransmitters of the adult striatum in vivo. Thus, cells of the adult mouse striatum have the capacity to divide and differentiate into neurons and astrocytes.
Substance P provoked gamma-aminobutyric acid release from the myenteric plexus of the guinea-pig small intestine
J Physiol 1985 May;362:319-29.PMID:2410602DOI:10.1113/jphysiol.1985.sp015680.
The release of [3H]gamma-aminobutyric acid (GABA) from the isolated small intestine of the guinea-pig pre-loaded with [3H]GABA was measured in the presence of Substance P and vasoactive intestinal polypeptide (VIP). Substance P (10(-10)-10(-7) M) produced a dose-dependent increase in the fractional rate of [3H]GABA release. VIP, even at 10(-7) M, did not affect the spontaneous [3H]GABA release nor the release of [3H]GABA evoked by electrical transmural stimulation (0.5 ms, 15 V, 10 Hz for 30 s). The release of endogenous GABA from the isolated small intestine was measured in the presence of Substance P (10(-9) M). After 60 min superfusion, the spontaneous release of GABA was 4.61 +/- 0.14 pmol min-1 g-1 wet wt. (n = 20). Substance P (10(-9) M) produced an approximate 2-fold spontaneous release of endogeneous GABA (8.74 +/- 0.21 pmol min-1 g-1 wet wt. (n = 10)). Perfusion with Ca-free medium containing 1 mM-EGTA and tetrodotoxin (3 X 10(-7) M) inhibited the release of endogenous GABA evoked by Substance P (10(-9) M). (D-Pro2, D-Trp7,9) Substance P (10(-6) M) antagonized the release of endogenous GABA evoked by Substance P (10(-9) M). These results indicate that Substance P induces a neuronal release of GABA through its receptor located in the guinea-pig small intestine. Substance P (10(-11)-10(-7) M) produced a dose-dependent increase in the fractional rate of [3H]acetylcholine (ACh) release from the isolated small intestine pre-loaded with [3H]choline. The release of [3H]ACh evoked by Substance P (10(-9) M) was inhibited by perfusion with Ca-free medium containing 1 mM-EGTA, tetrodotoxin (3 X 10(-7) M) and (D-Pro2, D-Trp7,9)Substance P (10(-6) M). Bicuculline (10(-6) M) inhibited the release of [3H]ACh evoked by Substance P (10(-9) M) by 68.1 +/- 4.6% (n = 5), thereby suggesting that the substance P-evoked ACh release is partly mediated through the endogenous GABA released by Substance P. These results provide evidence for the neurotransmitter role of GABA and a possible excitatory role of Substance P on the GABAergic neurones in the myenteric plexus of the guinea-pig small intestine.