CN112245415A - Application of 6-shogaol in preparation of medicine for treating cancer cachexia - Google Patents
Application of 6-shogaol in preparation of medicine for treating cancer cachexia Download PDFInfo
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- CN112245415A CN112245415A CN202011135328.6A CN202011135328A CN112245415A CN 112245415 A CN112245415 A CN 112245415A CN 202011135328 A CN202011135328 A CN 202011135328A CN 112245415 A CN112245415 A CN 112245415A
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Abstract
The invention provides application of 6-shogaol in preparing a medicament for treating cancer cachexia, wherein the effective component of the medicament is one or more of 6-shogaol, a hydrate of 6-shogaol, a pharmaceutically acceptable salt of 6-shogaol, a tautomer of 6-shogaol, a stereoisomer of 6-shogaol and a precursor compound of 6-shogaol. The 6-shogaol can relieve the inhibition effect of chemotherapy drugs capable of inducing cachexia on skeletal muscle differentiation, can reduce skeletal muscle degradation related protein, and provides a strategy for preparing drugs for treating cancer cachexia; in addition, the 6-shogaol has wide sources and low cost, and can be widely used for preparing the medicine for treating cancer cachexia.
Description
Technical Field
The invention relates to the field of biological medicine, in particular to application of 6-shogaol in preparing a medicine for treating cancer cachexia.
Background
Cancer cachexia is a complex disorder secondary to cancer with progressive systemic dysfunction and tissue atrophy. Cancer cachexia is caused by a variety of complex factors, with weight loss, anorexia, and asthenia as the main symptoms. Under the influence of systemic inflammation, increased resting energy expenditure in cachectic patients leads to increased muscle proteolysis and lipolysis, while anorexia further reduces energy intake and promotes cachexia progression. The overall quality of life of cancer cachexia patients is poor, with pain and fatigue, which severely affects the daily lives of the patients. Cachexia occurs in 50-85% of cancer patients, with high incidence in patients with pancreatic, intestinal, and lung cancers. Death cases directly caused by cancer cachexia exceed 700 million per year. It has been generally accepted that cancer cure can prevent cachexia, but weight loss continues for a long time even if the tumor is removed. Currently, there is no specific scheme for cancer cachexia worldwide. The development of a therapeutic approach to cancer cachexia is an important issue in overcoming the cancer cause.
At present, the treatment means of cancer cachexia mainly comprises drug therapy, nutritional support and physical exercise. Current therapeutic drugs are primarily appetite stimulants including corticosteroids, progestin analogs, cannabinoids, and 5-hydroxytryptamine antagonists. Only corticosteroids and progestogen analogs have been shown to be beneficial in alleviating the anorexia associated with this syndrome, and can increase the patient's appetite and weight without significantly affecting the patient's quality of life and survival. In addition, the clinical test result of the novel anticancer cachexia drug anamorelin stage III shows that the anticancer cachexia drug anamorelin can increase the appetite, the body weight and the muscle weight of a patient, but can not improve the muscle function and enhance the holding power, and has no obvious influence on the median survival time. Further evaluation work is required before large-scale clinical investment in anamorelin.
The occurrence of cancer cachexia is also associated with some common chemotherapy, targeted therapy. Folate treatment causes skeletal muscle atrophy and abnormal glucose metabolism in C26 colon cancer tumor-bearing mice, and aggravates inflammation. Cisplatin (DDP) acts on lung cancer-bearing mice to cause cachexia and acute kidney injury. Cisplatin action in rats causes anorexia, skeletal muscle atrophy, and significantly up-regulates plasma corticosterone levels. Cisplatin acting on colon cancer cachexia models did reduce tumor burden but did not improve muscle atrophy in mice, which was associated with activation of the NF-kappaB signaling pathway. Oxaliplatin and 5-fluorouracil can exacerbate muscle atrophy in C26 tumor-bearing mice, trigger autophagy, reduce protein synthesis, and induce mitochondrial changes. Etoposide (VP-16) can induce mouse macrophage to generate inflammatory cytokine, and cause cachexia related symptoms such as mouse anorexia, weight loss, inflammatory index up-regulation and the like.
The traditional Chinese medicine has a long clinical application history, has unique curative effect in antitumor treatment, and is mainly applied to traditional Chinese medicines and acupuncture, but is more popular in application. However, the traditional application methods of traditional Chinese medicines such as decoction also have the defects that the traditional Chinese medicines are difficult to overcome temporarily, such as difficult quality control and continuous change of prescription, so that the traditional Chinese medicines are difficult to popularize on a larger scale. Natural products represented by traditional Chinese medicines are a drug resource library to be developed, and many chemical drugs are derived from plant drugs, such as paclitaxel, berberine and the like. Many successful attempts have been made on the traditional Chinese medicine compound in treating cancer cachexia, and positive results are obtained in clinical trial evaluation of traditional Chinese medicine compounds or preparations such as nourishing vital qi and removing food retention capsules, ginseng and aconite injection, ginseng poria and bighead atractylodes rhizome powder and the like. The small molecular compound for resisting cancer cachexia is screened from the traditional Chinese medicine, and the small molecular compound is converted into a chemical drug, so that the method has important significance.
6-Shogaol (6-Shogaol, 6SH, molecular formula: C)17H24O3Molecular weight: 276.37g/mol) can be derived from rhizoma Pinelliae, rhizoma Zingiberis recens, and Zingiberis rhizoma. A plurality of in vivo and in vitro experimental researches show that the 6-shogaol has pharmacological activities of resisting neuritis, resisting tumor, stopping vomit and the like, and has certain medicinal potential.
Disclosure of Invention
Aiming at the defects of the prior art, the invention provides the application of 6-shogaol in preparing the medicine for treating cancer cachexia.
In order to achieve the purpose, the invention adopts the following technical scheme:
the first aspect of the invention provides an application of 6-shogaol in preparing a medicament for treating cancer cachexia, wherein the effective component of the medicament is one or more of 6-shogaol, a hydrate of 6-shogaol, a pharmaceutically acceptable salt of 6-shogaol, a tautomer of 6-shogaol, a stereoisomer of 6-shogaol and a precursor compound of 6-shogaol.
Further, the cancer is colon cancer or lung cancer.
Further, the administration route of the drug is oral, transdermal, intramuscular, subcutaneous or intravenous injection.
Furthermore, the medicament can be prepared into tablets, capsules, oral liquid, buccal agents, granules, medicinal granules, pills, powder, paste, pellets, suspensions, powder, solutions, injections, suppositories, creams, sprays, drops or patches.
Further, the medicine also comprises a pharmaceutically acceptable carrier or excipient.
Further, the excipient comprises one or more of a binder, a filler, a diluent, a tabletting agent, a lubricant, a disintegrating agent, a coloring agent, a flavoring agent and a wetting agent.
The second aspect of the invention provides a medicament for treating cancer cachexia, which comprises one or more of 6-shogaol, a hydrate of 6-shogaol, a pharmaceutically acceptable salt of 6-shogaol, a tautomer of 6-shogaol, a stereoisomer of 6-shogaol and a precursor compound of 6-shogaol.
Further, the cancer is colon cancer or lung cancer.
The third aspect of the invention provides the application of 6-shogaol in preparing the medicine for inhibiting the proliferation of tumor cells and relieving the atrophy of myotube protein.
The fourth aspect of the invention provides application of 6-shogaol in preparing a medicament for down-regulating the expression of ubiquitin-proteasome pathway related protein MAFbx in skeletal muscle.
By adopting the technical scheme, compared with the prior art, the invention has the following technical effects:
the research results of the invention show that: the 6-shogaol has good inhibition effect on mouse lung cancer LLC cells and mouse colon cancer CT26 cells when acting for 24h, 48h and 72h in vitro, and has no obvious proliferation inhibition effect on mouse fibroblast c2c12 cells. 6-shogaol reduced cisplatin-induced atrophy of c2c12 myocyte cells, indicating that 6-shogaol reduced inhibition of skeletal muscle differentiation by chemotherapeutic drugs capable of inducing cachexia. In vivo experiments, 6-shogaol can relieve cachexia symptoms of LLC tumor-bearing mice under cisplatin treatment, such as weight loss, food intake reduction, skeletal muscle weight reduction, kidney weight reduction, epididymal fat weight reduction and the like; and simultaneously, the expression of ubiquitin-proteasome pathway related protein MAFbx in skeletal muscle is reduced.
In conclusion, the 6-shogaol can relieve the inhibition effect of chemotherapy drugs capable of inducing cachexia on skeletal muscle differentiation, can down-regulate skeletal muscle degradation related protein, and provides a strategy for preparing drugs for treating cancer cachexia; in addition, the 6-shogaol has wide sources and low cost, and can be widely used for preparing the medicine for treating cancer cachexia.
Drawings
FIG. 1 is a graph showing the effect of various concentrations of 6-shogaol on proliferation of mouse fibroblast c2c12 cells in accordance with one embodiment of the present invention;
FIG. 2 is a graph showing the effect of various concentrations of 6-shogaol on proliferation of mouse colon cancer CT26 cells in accordance with an embodiment of the present invention;
FIG. 3 is a graph showing the effect of different concentrations of 6-shogaol on the proliferation of mouse lung cancer LLC cells in one embodiment of the invention;
FIG. 4 is a graph showing the effect of 6-shogaol on the differentiation of myocyte of cisplatin-stimulated mouse c2c12 in accordance with an embodiment of the present invention;
FIG. 5 is a bar graph of the effect of 6-shogaol on the differentiation of myocyte cells of cisplatin-stimulated mouse c2c12 in accordance with an embodiment of the present invention;
FIG. 6 is a graph showing the effect of 6-shogaol on MYOG protein expression in cisplatin-stimulated mouse c2c12 myocyte MYOG cells in one example of the invention; wherein, the graph A is a WB result graph of the effect of 6-shogaol on MYOG protein expression, and the graph B is a bar chart of relative expression of MYOG protein in different treatment groups;
FIG. 7 is a graph showing the effect of 6-shogaol on the body weight (panel A), tumor mass volume (panel B), and food intake (panel C) of LLC tumor-bearing mice treated with cisplatin in accordance with an embodiment of the present invention;
FIG. 8 is a graph showing the effect of 6-shogaol on tumor weight (panel A), food intake (panel B), gastrocnemius weight (panel C), tibialis anterior muscle weight (panel D), kidney weight (panel E), epididymal fat weight (panel F) in cisplatin-treated LLC tumor-bearing mice in accordance with one embodiment of the present invention;
FIG. 9 is a graph showing the effect of 6-shogaol on the cross-sectional area of the gastrocnemius muscle fibers of LLC tumor-bearing mice treated with cisplatin according to one embodiment of the present invention, wherein A is the result of staining 6-shogaol on the cross-sectional area HE of the gastrocnemius muscle fibers of LLC tumor-bearing mice treated with cisplatin, B is the result of the cross-sectional area distribution of the gastrocnemius muscle fibers, and C is a histogram of the cross-sectional area of the gastrocnemius muscle fibers;
FIG. 10 is a graph showing the effect of 6-shogaol on the expression of MAFbx protein in gastrocnemius muscle of LLC tumor-bearing mice treated with cisplatin in accordance with an embodiment of the present invention; wherein, the graph A is a WB result of the effect of MAFbx protein expression in gastrocnemius, and the graph B is a histogram of the relative expression of MAFbx protein.
Detailed Description
The invention provides application of 6-shogaol in preparing a medicament for treating cancer cachexia, wherein the effective component of the medicament is one or more of 6-shogaol, a hydrate of 6-shogaol, a pharmaceutically acceptable salt of 6-shogaol, a tautomer of 6-shogaol, a stereoisomer of 6-shogaol and a precursor compound of 6-shogaol.
In a preferred embodiment of the invention, the cancer is colon cancer or lung cancer.
In a preferred embodiment of the invention, the route of administration of the drug is oral, transdermal, intramuscular, subcutaneous or intravenous injection.
In a preferred embodiment of the invention, the medicament is in the form of tablets, capsules, oral liquid, buccal agents, granules, medicinal granules, pills, powder, ointment, pellets, suspensions, powder, solutions, injections, suppositories, creams, sprays, drops or patches.
In a preferred embodiment of the present invention, the excipient includes one or more of a binder, a filler, a diluent, a tabletting agent, a lubricant, a disintegrating agent, a coloring agent, a flavoring agent, and a humectant.
Wherein, the term "pharmaceutically acceptable salt" refers to a salt of the compound with a pharmaceutically acceptable inorganic or organic acid, including but not limited to: hydrochloric acid, hydrobromic acid, phosphoric acid, nitric acid, sulfuric acid; such organic acids include, but are not limited to: formic acid, acetic acid, propionic acid, succinic acid, 1, 5-naphthalenedisulfonic acid, sulfinic acid, oxalic acid, tartaric acid, lactic acid, salicylic acid, benzoic acid, valeric acid, diethylacetic acid, malonic acid, succinic acid, fumaric acid, pimelic acid, adipic acid, maleic acid, malic acid, sulfamic acid, phenylpropionic acid, gluconic acid, ascorbic acid, nicotinic acid, isonicotinic acid, methanesulfonic acid, p-toluenesulfonic acid, citric acid, and amino acids; by "pharmaceutically acceptable" is meant a material that is suitable for use in humans without undue adverse side effects (such as toxicity, irritation, and allergic response), i.e., at a reasonable benefit/risk ratio.
The term "tautomer" refers to a functional group isomer resulting from the rapid movement of an atom in a molecule at two positions, for example: enols and the corresponding ketones.
The term "stereoisomer" refers to isomers resulting from the different arrangement of atoms in a molecule, such as: cis-trans isomers, enantiomers, conformers, and the like.
The term "precursor compound" refers to a compound which is inactive in vitro, but can be converted into the active ingredient of the present invention by metabolic or chemical reaction in vivo, thereby exerting its pharmacological effect.
The present invention will be described in detail and specifically with reference to the following examples and drawings so as to provide a better understanding of the invention, but the following examples do not limit the scope of the invention.
In the examples, the conventional methods were used unless otherwise specified, and reagents used were those conventionally commercially available or formulated according to the conventional methods without specifically specified.
Example 1
This example provides a research experiment of 6-shogaol inhibiting mouse fibroblast c2c12 cell proliferation, and the specific experimental contents and results are as follows:
6-shogaol with different concentrations and mouse fibroblast c2c12 cells were co-cultured for 24, 48 and 72 hours, and the number of living cells was detected by CCK8 experiment, and the results are shown in FIG. 1: according to the curve trend, the weak inhibition effect of 6-shogaol on the activity of c2c12 cells at 24h, 48h and 72h can be preliminarily judged; the IC50 of 6-shogaol on c2c12 cells at 72h is only 912.98 μ M; 6-shogaol has no obvious influence on the proliferation of c2c12 cells in 24h, 48h and 72 h.
Example 2
This example demonstrates the inhibitory effect of 6-shogaol on mouse colon cancer CT26 cell proliferation, and the specific experimental contents and results are as follows:
co-culturing 6-shogaol with different concentrations and mouse colon cancer CT26 cells for 24, 48 and 72 hours, and detecting the number of living cells by using a CCK8 experiment, wherein the results are shown in figure 2, and the IC50 of the 6-shogaol to the CT26 cells at 24 hours, 48 hours and 72 hours are 903.04 mu M, 762.04 mu M and 26.27 mu M respectively; 6-shogaol has no obvious influence on LLC cell proliferation in 24h and 48h, and has good proliferation inhibition effect in 72 h.
Example 3
This example demonstrates the inhibitory effect of 6-shogaol on mouse lung cancer LLC cell proliferation, and the specific experimental contents and results are as follows:
6-shogaol with different concentrations and mouse lung cancer LLC cells are co-cultured for 24, 48 and 72 hours, and the number of living cells is detected by a CCK8 experiment, and the results are shown in figure 3, wherein the IC50 of 6-shogaol to LLC cells at 24 hours, 48 hours and 72 hours is 738.23 mu M, 658.77 mu M and 365.10 mu M respectively. The 6-shogaol has a relatively common inhibition effect on LLC cell proliferation in 24h, 48h and 72 h.
Example 4
This example demonstrates the inhibitory effect of 6-shogaol on cisplatin-stimulated myocyte differentiation in mouse c2c12, and the specific experimental contents and results are as follows:
mouse fibroblast c2c12 cells were induced to differentiate into myotube cells by 2% horse serum, incubated with c2c12 myotube cells for 24 hours with different concentrations of 6-shogaol and 40 μ M cisplatin (DDP), fixed, permeabilized, blocked, incubated with MyHC-primary antibody at 4 ℃ overnight, incubated with primary antibody, washed and incubated with homofluorescent secondary antibody for 2 hours, incubated with secondary antibody, washed, incubated with DAPI for nuclear staining, incubated for 10 minutes, washed, covered with anti-fluorescent quencher, and finally photographed by fluorescence microscope, with the results shown in fig. 4, and the fluorescence regions shown in fig. 4 were counted as shown in fig. 5 (P < 0.05, # P < 0.01, # P < 0.001, the same below). As is clear from FIGS. 4 and 5, the myotube area of the c2c12 myotube cells was significantly decreased and atrophy occurred after 24 hours of DDP treatment. The MyHC-labeled myotube cell area gradually increased with increasing 6-shogaol concentration, reflecting that 6-shogaol can alleviate DDP-induced c2c12 myotube cell atrophy and shows concentration dependence.
Example 5
This example demonstrates the effect of 6-shogaol on the upregulation of MYOG protein expression in cisplatin-stimulated myocyte cells of mouse c2c12, and the specific experimental contents and results are as follows:
mouse fibroblast c2c12 cells are induced and differentiated into myotube cells by 2% horse serum, 6-shogaol with different concentrations and 40 mu M cis-platinum are co-cultured with c2c12 myotube cells for 24 hours, RIPA lysate is used for extracting total protein, protein concentration of each sample is leveled after protein concentration is measured by BCA method, expression of myodifferentiation related protein MYOG is detected by western blot method, and the result is shown in figure 6. After the c2c12 myotube cells are treated by DDP for 24 hours, the expression level of MYOG protein is obviously reduced, and the expression of MYOG is obviously up-regulated under the intervention of 6-shogaol.
Example 6
This example demonstrates the effect of 6-shogaol on reduction of signs of cachexia-related symptoms in cisplatin-treated LLC tumor-bearing mice, and the specific experimental contents and results are as follows:
LLC cells (2X 10)6One cell/one) was subcutaneously inoculated on the right upper back of 20C 57BL/6 mice at day1, and the 20 tumor-bearing mice were divided into four groups, each of which was 5, namely tumor-bearing control group (LLC group), cisplatin-treated group (LLC + DDP group), cisplatin-low-dose 6-shogaol-combination-treated group (LLC + DDP +6sh (l) group), cisplatin-high-dose 6-shogaol-combination-treated group (LLC + DDP +6sh (h) and 5C 57 mice of the same batch served as normal control group (NC group). After the tumor reaches 5mm in length (about 5 days), the administration is started, and the administration mode is intraperitoneal injection. The administration scheme is as follows: NC group (normal saline), LLC + DDP group (DDP 4mg/kg), LLC + DDP +6SH (L) (DDP4mg/kg +6SH5mg/kg), LLC + DDP +6SH (H) (DDP4mg/kg +6SH10mg/kg), and the administration cycles are all 3 days and 1 time.Body weight, tumor size, body weight and tumor trend are shown in fig. 7. DDP can obviously reduce the weight of a mouse, and the influence of cisplatin on the weight and the food intake can be reduced through the intervention of 6-shogaol.
All mice were sacrificed on day 18 and examined for tumor weight, gastrocnemius muscle weight, tibialis anterior muscle weight, kidney weight and epididymal fat weight, the results are shown in fig. 8. After 6-shogaol intervention, the total body weight of the mice tends to be increased relative to the DDP group, and the weights of gastrocnemius, tibialis anterior muscle, kidney and epididymis fat are obviously increased. The cross-sectional area of the gastrocnemius muscle fiber of the mice was significantly increased after the intervention of 6-shogaol, as shown in fig. 9. Total protein was extracted from gastrocnemius muscle, and expression of MAFbx protein was detected by western blot method, as shown in fig. 10. Intervention of 6-shogaol significantly inhibited the expression of MAFbx protein relative to the DDP group.
The above examples show that 6-shogaol can relieve the inhibition effect of chemotherapy drugs capable of inducing cachexia on skeletal muscle differentiation, can down-regulate the expression of skeletal muscle degradation-related proteins, and provides a strategy for preparing drugs for treating cancer cachexia.
The embodiments of the present invention have been described in detail, but the embodiments are merely examples, and the present invention is not limited to the embodiments described above. Any equivalent modifications and substitutions to those skilled in the art are also within the scope of the present invention. Accordingly, equivalent changes and modifications made without departing from the spirit and scope of the present invention should be covered by the present invention.
Claims (10)
- The application of 6-shogaol in preparing the medicine for treating cancer cachexia is characterized in that the effective component of the medicine is one or more of 6-shogaol, hydrate of 6-shogaol, pharmaceutically acceptable salt of 6-shogaol, tautomer of 6-shogaol, stereoisomer of 6-shogaol and precursor compound of 6-shogaol.
- 2. The use of claim 1, wherein the cancer is colon cancer or lung cancer.
- 3. The use according to claim 1, wherein the drug is administered orally, transdermally, intramuscularly, subcutaneously or intravenously.
- 4. The use according to claim 1, wherein the medicament is in the form of tablets, capsules, oral liquids, buccal agents, granules, electuary, pills, powders, ointments, pellets, suspensions, powders, solutions, injections, suppositories, creams, sprays, drops or patches.
- 5. The use of claim 1, wherein the medicament further comprises a pharmaceutically acceptable carrier or excipient.
- 6. The use according to claim 5, wherein the excipient comprises one or more of a binder, a filler, a diluent, a tableting agent, a lubricant, a disintegrant, a colouring agent, a flavouring agent, a humectant.
- 7. A medicine for treating cancer cachexia is characterized by comprising one or more of 6-shogaol, a hydrate of 6-shogaol, a pharmaceutically acceptable salt of 6-shogaol, a tautomer of 6-shogaol, a stereoisomer of 6-shogaol and a precursor compound of 6-shogaol.
- 8. The medicament for treating cancer cachexia of claim 7, wherein said cancer is colon cancer or lung cancer.
- 9.6-shogaol is used in preparing medicine for inhibiting tumor cell proliferation and relieving myotube protein atrophy.
- 10.6-shogaol in the preparation of drugs for down-regulating the expression of ubiquitin-proteasome pathway associated protein MAFbx in skeletal muscle.
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Cited By (1)
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| CN115040536A (en) * | 2022-07-13 | 2022-09-13 | 新疆医科大学 | Pharmaceutical composition with synergistic non-small cell lung cancer resisting effect and application thereof |
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| US20070071838A1 (en) * | 2005-09-27 | 2007-03-29 | The Quigley Corporation | Method for the treatment of cachexia |
| WO2018129315A1 (en) * | 2017-01-06 | 2018-07-12 | Flex Pharma, Inc. | Methods and compositions for the treatment of disease |
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