CN115990179A - Application of hesperidin in preparation of medicine for treating chronic obstructive pulmonary disease - Google Patents
Application of hesperidin in preparation of medicine for treating chronic obstructive pulmonary disease Download PDFInfo
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- CN115990179A CN115990179A CN202211623360.8A CN202211623360A CN115990179A CN 115990179 A CN115990179 A CN 115990179A CN 202211623360 A CN202211623360 A CN 202211623360A CN 115990179 A CN115990179 A CN 115990179A
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- Prior art keywords
- hesperidin
- hsd
- obstructive pulmonary
- chronic obstructive
- pulmonary disease
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Abstract
The invention relates to the technical field of medicines, in particular to application of hesperidin in preparation of medicines for treating chronic obstructive pulmonary disease, wherein the hesperidin has remarkable wide anti-inflammatory effect, has the effects of relieving cough and reducing phlegm, can improve chronic inflammation of chronic obstructive pulmonary disease, and can effectively improve symptoms of chronic cough and chronic expectoration of patients. Therefore, the hesperidin is developed into a product for treating chronic obstructive pulmonary disease, and has wide application prospect and good economic and social benefits.
Description
Technical Field
The invention relates to the technical field of medicines, in particular to application of hesperidin in preparation of a medicine for treating chronic obstructive pulmonary disease.
Technical Field
Respiratory diseases are of many kinds and can be divided into two major categories, infectious diseases and non-infectious diseases. Respiratory diseases such as various types of pneumonia, bronchitis, phthisis, novel coronavirus pneumonia and the like in 2019 outbreak are all caused by biological factors such as bacteria, viruses and the like, while chronic obstructive pulmonary diseases are mainly caused by abiotic factors such as smoking, air pollution, occupational exposure and the like, and antiviral and antibacterial drugs commonly used for treating respiratory diseases caused by biological factors are almost ineffective for treating the chronic obstructive pulmonary diseases.
Chronic obstructive pulmonary disease (Chronic obstructive pulmonary disease, hereinafter referred to as COPD or chinese chronic obstructive pulmonary disease) is a common, preventable, treatable disease, generally caused by abnormalities of the airways and/or alveoli caused by prolonged exposure to toxic particles or gases, and is affected by host factors such as dysplasia of the lungs, characterized by airflow limitation and sustained respiratory symptoms.
The related data published by the world health organization show that slow pulmonary resistance has become the third leading cause of death worldwide after ischemic heart disease, stroke, accounting for 6% of the total number of deaths worldwide in 2019, where 90% of deaths occur in low and medium income countries, closely related to toxic particulates or gases that come into long-term contact with smoking, air pollution, professional exposure, etc. With the rapid development of industrial economy, continuous increase of smoking rate and aging of population in China, slow-resistance lung patients in China are increased, about 1 hundred million slow-resistance lung patients exist at present, and the prevalence rate of people over 60 years old exceeds 27%. Since the prevalence and mortality of patients with chronic obstructive pulmonary disease remain high, the patient's labor and quality of life are seriously affected, and repeated occurrences and visits have created a great social and economic burden.
Smoke inhalation is a major causative factor of slow resistance to the lungs, an important risk factor for inducing inflammation of the respiratory tract and lungs, and a preventable important risk factor for causing death of humans worldwide. There are 69 known carcinogens in tobacco smoke, among which harmful substances such as nicotine, tar, heavy metals, free radicals and the like destroy cilia of airway epithelium and impair airway mucus removing function; the sensitivity of cough reflex of the organism is reduced, and the respiratory tract clearing function is weakened; inducing activation of lung epithelial cells and vascular endothelial cells, stimulating secretion of various inflammatory cytokines (such as TNF-alpha and IL-1 beta) and chemokines, inducing immune cells to excessively gather in airway and lung tissues, further inducing chronic inflammation, and continuing inflammatory reaction to damage airway and lung parenchyma, further causing continuous airflow obstruction, and forming chronic diseases such as chronic obstructive pulmonary disease.
Air pollution includes indoor air pollution and outdoor air pollution. Indoor air pollution mainly comes from smoking and incomplete combustion of household fuel, is an important risk factor for slow lung resistance illness and death, and is alsoOne of the first ten risk factors that create a global economic burden. Harmful substances such as carbon monoxide, nitrogen oxides, sulfur-containing oxides and the like polluted by indoor air act on lung epithelial cells and vascular endothelial cells for a long time, so that persistent inflammatory injury of the airway and the lung is caused, and the risk of chronic obstructive pulmonary disease is increased. The outdoor air pollution mainly comprises PM 10 、PM 2.5 Isoasol state contaminants and O 3 、SO 2 、NO 2 Gaseous pollutants such as CO and the like are another important factor for increasing the risk of chronic obstructive pulmonary disease and are also important reasons for acute exacerbation of patients with chronic obstructive pulmonary disease. The prevalence of slow lung resistance increases by about 6% per unit increase in the concentration of Particulate Matter (PM), sulfur dioxide, etc. contaminants in the air. Air pollutants directly enter human body through respiratory tract and PM 10 Can be deposited in the upper airway, PM 2.5 Can be deposited in the lower airway, and the gaseous pollutants directly act on alveoli to trigger respiratory chronic inflammation by activating oxidative stress, promoting anti-inflammatory reaction, inducing apoptosis and other ways, thereby causing respiratory symptoms and lung function damage and increasing the risk of slow pulmonary obstruction and acute exacerbation. The more serious the air pollution, the higher the incidence of slow pulmonary resistance, and especially the excessive contact with air pollution in childhood, the greater the influence on the pulmonary function.
Occupational exposure such as dust, toxic gases and the like is also an important causative factor of slow lung obstruction like smoking and air pollution. Long-term inhalation of dust can deposit in the respiratory system of a patient, cause ciliated damage to the respiratory tract epithelium and reduced sensitivity to cough, and gradually reduce the respiratory tract clearance function. Studies have shown that professional exposure personnel such as dust, toxic gases, etc. are 1.6 times more at risk of having a slow lung obstruction than non-exposure persons. Long-term occupational exposure, which causes continuous stimulation of the respiratory system, causes chronic inflammation of the respiratory system and the body, and increases the risk of chronic obstructive pulmonary disease.
Chronic obstructive pulmonary disease is a chronic respiratory disease that is a serious health hazard, the pathogenesis is complex, and current research on pathogenesis is mainly focused on chronic inflammation. After the harmful gas or particles enter the airway and lung tissues, the mode recognition receptor (Pattern recognition receptor, PRR) is triggered to activate innate immune cells such as macrophages, neutrophils, eosinophils and the like and structural cells in the airway of epithelial cells, endothelial cells and fibroblasts, and directly or indirectly activate the inflammation-related injury molecular mode, so that various cytokines, chemokines, acute phase response proteins and the like are released. Such as increased macrophages, promote the release of inflammatory and chemotactic factors, including TNF- α, IL-1 β, etc., which promote recruitment of inflammatory cells such as neutrophils and monocytes to the lungs and promote maturation of macrophages, alveolar macrophages secrete elastase, promote enhanced inflammation, while the number of activated neutrophils increases, release elastase, cathepsin G, MMP-8, MMP-9, cysteine proteases, etc., promote mucus hypersecretion, alveolar interstitial and pulmonary parenchyma destruction, resulting in sustained inflammatory responses of the airways and lungs, promote the progression of slow obstructive lungs.
Chronic obstructive pulmonary disease is mainly caused by abiotic factors such as smoking, air pollution, occupational exposure, etc., and antiviral and antibacterial drugs commonly used for treating respiratory diseases caused by biological factors are almost ineffective for treating chronic obstructive pulmonary disease. Due to the industrial development, traffic pollution, continuously rising smoking rate and other reasons, air pollution is more and more serious, and people face toxic gases or particles in the air to continuously stimulate the respiratory system, stimulate the airway and the lung to generate chronic inflammation, and further develop into chronic obstructive pulmonary diseases no matter indoors or outdoors.
Hesperidin (HSD) is a flavonoid compound, and is mainly extracted from citrus fruits. Is extremely insoluble in water at normal temperature, is almost insoluble in acetone, benzene and chloroform, is easily soluble in dilute alkali solution, has no odor and smell, and widely exists in citrus fruits. It has antioxidant, antiinflammatory, antibacterial and anticancer activities, and can be widely used in medicine and food science fields.
Modern pharmacological studies show that hesperidin has the function of preventing and treating respiratory diseases caused by biological factors such as viruses or bacteria. Zhao Xingyan it has been shown by studies that hesperidin may promote macrophage M2 type polarization by inhibiting the Jagged1/Notch1 pathway to reduce lung injury caused by respiratory syncytial virus (Zhao Xingyan, shang Zhengzhen, yue Chun, tan Zongping, huang Bo. Hesperidin regulates the effect of Jagged1/Notch1 pathway on macrophage polarization and bronchiolitis mouse lung injury, proc. Natl. Acad. Sci. China, 2022,44 (05): 777-784.). Zhou Zheng et al found that hesperidin reduced bleomycin-induced idiopathic pulmonary fibrosis by inhibiting TGF-. Beta.1/Smad 3/AMPK and IκBα/NF-. Kappa.B pathways, thereby improving the modulation of oxidative and pro-inflammatory markers (Nrf 2 and HO-1) and (TNF-. Alpha., IL-1β, IL-6), reducing collagen deposition during pulmonary fibrosis (Zhou Zheng, kandhare Amit D, kandhare Anwesha A, bodhankar Subhash L. Hesperidin ameliorates bleomycin-induced experimental pulmonary fibrosis via inhibition of TGF-beta1/Smad3/AMPK and IkappaBalpha/NF-kappa B pathies. EXCLI journ, 2019,18.). Any Zhou Xin and the like invent application of hesperidin in preparing medicines for preventing and/or treating pulmonary fibrosis diseases, and the patent shows that the hesperidin is used for preventing and treating pulmonary fibrosis by inhibiting proliferation of pulmonary fibroblasts and epithelial-mesenchymal transition of alveolar epithelial cells and inhibiting activation of the pulmonary fibroblasts (any Zhou Xin, chen Yulong, wu Zhaoyu, feng Suxiang, zhoujiang. Application of hesperidin in preparing medicines for preventing and/or treating pulmonary fibrosis diseases: henan: CN104906120A, 2015-09-16.).
However, there is no related product developed from orange peel for treating slow pulmonary obstruction caused by abiotic factors such as smoking and air pollution in the market, and no related document reports that the medicinal value of orange peel is not fully exerted.
Disclosure of Invention
The invention aims to overcome the technical problems in the prior art and provides application of hesperidin in preparation of a medicament for treating chronic obstructive pulmonary disease.
The aim of the invention is achieved by the following scheme:
application of hesperidin in preparing medicine for treating chronic obstructive pulmonary disease is provided.
The chemical formula of the hesperidin is as follows:
english name of hesperidin: hesperidin; molecular weight: 610.56; the molecular formula: c (C) 28 H 34 O 15 。
Preferably, in said use, the medicament comprises hesperidin and one or more pharmaceutically acceptable excipients.
Preferably, in said application, the amount of hesperidin in said medicament is between 1 and 100mg/kg.
Preferably, in said application, the amount of hesperidin in said medicament is between 5 and 90mg/kg.
Preferably, in said application, the amount of hesperidin in said medicament is between 10 and 40mg/kg.
Preferably, in said application, said auxiliary material comprises: starch, soluble starch, microcrystalline cellulose, magnesium stearate, lactose, dextrin, hydroxypropyl methylcellulose, and talc.
Preferably, in the application, the medicament is a tablet, a capsule, a granule, a powder, an oral liquid, a granule or a pill.
Compared with the prior art, the invention has the following technical effects:
the application of the hesperidin in preparing the medicine for treating the chronic obstructive pulmonary disease disclosed by the invention has remarkable wide anti-inflammatory effect, has the effects of relieving cough and reducing phlegm, can improve chronic inflammation of the chronic obstructive pulmonary disease, and can effectively improve the symptoms of chronic cough and chronic expectoration of patients. Therefore, the hesperidin is developed into a product which has few medicinal ingredients and definite curative effect and is used for treating the chronic obstructive pulmonary disease, has wide application prospect and good economic and social benefits, and has important theoretical and practical significance.
Drawings
FIG. 1 is a graph showing the results of cough latency in mice;
FIG. 2 shows the results of cough count in 5min in mice;
FIG. 3 shows the results of serum TNF- α assay in a mouse antitussive assay;
FIG. 4 shows serum IL-1. Beta. Assay results in a mouse antitussive assay;
FIG. 5 shows the measurement results of phenol red standard curve;
FIG. 6 shows the results of sputum excretion measurements in mice;
FIG. 7 shows the results of serum TNF- α assay in a mouse sputum elimination assay;
FIG. 8 shows serum IL-1. Beta. Measurement results in a mouse phlegm eliminating experiment;
FIG. 9 shows the results of measurement of ear swelling degree of mice;
FIG. 10 shows the results of serum TNF- α assay in a mouse anti-inflammatory assay;
FIG. 11 shows serum IL-1. Beta. Assay results in a mouse anti-inflammatory assay;
(ns represents P > 0.05, <0.01, <0.001, <0.0001, < P).
Detailed Description
In order to make the objects, technical solutions and advantages of the present invention more apparent, the technical solutions of the present invention will be described in detail with reference to specific examples and comparative examples. It will be apparent that the described embodiments are only some, but not all, embodiments of the invention. All other embodiments, based on the examples herein, which are within the scope of the invention as defined by the claims, will be within the scope of the invention as defined by the claims.
Except for the special description, the equipment used in the embodiment is conventional experimental equipment, and the materials and reagents used are all obtained in the market unless the special description is made, and the experimental method without the special description is also conventional experimental method.
Example 1
Mixing sodium hydroxymethyl cellulose as adjuvant with hesperidin, and making into oral liquid. The dose of Hesperidin (HSD) was 10mg/kg (low dose), 20mg/kg (medium dose) and 40mg/kg (high dose), respectively.
Experimental example 1: cough test
(1) Grouping and administration of animals
30 SPF-class 4-week-old ICR male mice were obtained and supplied from the university of Zhongshan (the center of laboratory animals, east campus), and the laboratory animals were given license numbers: SCXK (Yue) 2021-0029. ICR mice were divided into 5 groups, namely, hesperidin low dose group (HSD-L, 10 mg/kg), hesperidin medium dose group (HSD-M, 20 mg/kg), hesperidin high dose group (HSD-H, 40 mg/kg), positive drug control group (pentovirine, PV,50 mg/kg), negative control group (0.5% sodium carboxymethyl cellulose, CMC-Na). All drugs were first dissolved in 0.5% sodium carboxymethyl cellulose solution and diluted to the desired concentration depending on the dose. The administration mode is gastric lavage administration.
(2) Model creation and evaluation
The method comprises the following steps of firstly adapting to the environment for 3 days, carrying out gastric lavage for 7 days, carrying out no water control after 12 hours before administration on the last day, putting the mice into a 1000mL glass bell jar after administration for 1 hour on the last day, uniformly spraying 0.3mL of strong ammonia water into the glass bell jar for 30 seconds at the maximum flow rate by using an ultrasonic atomizer, and observing and recording the incubation period of the cough (the time from spraying ammonia water to first cough) of the mice and the times of cough (abdominal muscle contraction, opening mouth and accompanying cough sound) within 5 minutes. And (3) taking blood from eyeballs, removing necks, killing, standing the blood, and centrifuging to obtain serum for detecting the expression quantity of blood inflammatory factors. The time of the incubation period of the cough and the times of the cough are used as evaluation indexes of the cough relieving efficacy, and the expression quantity of the serum inflammatory factors is used as an evaluation index of wide anti-inflammatory.
(3) Experimental results
As shown in the results of the cough latency period of the mice in fig. 1, PV (62.17±2.17) s, HSD-H (76.67±2.78) s, HSD-M (55.33 ±1.45) s were prolonged by 532.42% (< 0.0001) and 679.93% (< 0.0001) and 462.90% (< 0.0001) respectively, compared with CMC-Na (9.83±2.17) s, which had a statistical significance, significantly prolonged the cough latency period of the mice, and HSD-L (15.50±1.34) s was prolonged by 57.68% (ns) compared with CMC-Na cough latency period, without significant differences.
As shown in the cough count results of 5min in the mice of fig. 2, PV (46.83±2.33), HSD-H (52.83±2.85), HSD-M (105.00±1.44), HSD-L (164.67±2.95) were reduced by 79.97% (< 0.0001) and 77.41% (< 0.0001) and 55.10% (< 0.0001) respectively, and the PV and HSD were statistically significant in reducing the cough count in the mice.
TNF-alpha and IL-1β are key mediators of inflammation. As shown in the measurement results of TNF- α in mouse serum of fig. 3, PV (552.00 ±79.39) pg/mL, HSD-H (249.78 ± 42.64) pg/mL, HSD-M (387.56 ±55.56) pg/mL, HSD-L (909.78 ± 70.10) pg/mL, the content of anti-inflammatory factor TNF- α in serum was reduced by 62.10% (P < 0.0001), 82.85% (P < 0.0001), 73.39% (P < 0.0001), and 37.53% (P < 0.01), respectively, and the content of TNF- α in serum was significantly reduced by 62.10% (P < 0.0001), respectively, which is statistically significant.
As shown in the measurement results of IL-1β in mouse serum of fig. 4, PV (168.20 ±5.66) pg/mL, HSD-H (152.71 ±2.48) pg/mL, HSD-M (182.71 ±1.95) pg/mL, HSD-L (232.31 ±6.80) pg/mL, the content of anti-inflammatory factor IL-1β in serum was reduced by 48.13% (< 0.0001) P, 52.91% (< 0.0001) P, 43.66% (< 0.0001) P, 28.36% (< 0.001) P, and PV and HSD significantly reduced the content of IL-1β in serum, respectively, which is statistically significant.
Experimental example 2: phlegm eliminating experiment
(1) Grouping and administration of animals
30 SPF-class 4-week-old ICR male mice were obtained and supplied from the university of Zhongshan (the center of laboratory animals, east campus), and the laboratory animals were given license numbers: SCXK (Yue) 2021-0029. ICR mice were divided into 5 groups, namely, HSD-L, HSD-M, HSD-H, positive drug control group (ambroxol hydrochloride, AM) and negative control group (CMC-Na), wherein the doses of the HSD-L, HSD-M, HSD-H administered were 10mg/kg, 20mg/kg and 40mg/kg, respectively, the positive control group was administered with ambroxol hydrochloride (AM) 15mg/kg, and the negative drug control group was administered with 0.5% sodium carboxymethyl cellulose (CMC-Na). All drugs were first dissolved in 0.5% sodium carboxymethyl cellulose solution and diluted to the desired concentration depending on the dose. The administration mode is gastric lavage administration.
(2) Configuration of phenol red standard curve
Precisely weighing phenol red 0.05g in a 50mL volumetric flask, preparing solution A by using 1mol/L sodium hydroxide solution and 0.9% sodium chloride solution according to the ratio of 1:15, and dissolving, and fixing the volume to serve as a storagePreparing liquid. Diluting with A solution to 2.00 μg/mL, 1.75 μg/mL, 1.50 μg/mL, 1.25 μg/mL, 1.00 μg/mL, 0.75 μg/mL, 0.50 μg/mL, 0.25 μg/mL, 0 μg/mL, and measuring absorbance (A) at 558.5nm on ultraviolet-visible spectrophotometer, measuring the concentration in parallel for 3 times, taking average value, linearly regressing mass concentration (C) with average value of A to obtain phenol red standard curve y=0.1543x, R 2 =0.9998, as shown in fig. 5.
(3) Model creation and evaluation
Firstly adapting to the environment for 3 days, carrying out gastric lavage for 7 days, carrying out no water forbidden after 12 hours before administration on the last day, carrying out intraperitoneal injection of 5% phenol red (w/v physiological saline) at a dosage of 0.2mL/20g after administration for 0.5 hour, taking out the eyeball after 0.5 hour, removing the neck for sacrifice, separating the trachea (cut from the lower edge of thyroid cartilage and the bifurcation of the trachea) and soaking in the A solution for ultrasonic treatment for 10 minutes (absorbance at 558.5 nm), and centrifuging to obtain serum after standing the blood for detection of the expression quantity of blood inflammatory factors. The phenol red excretion concentration was obtained by conversion from a phenol red standard curve, and the phlegm eliminating index was the increase rate (IR%) of the phenol red excretion concentration. Phenol red excretion concentration and an phlegm eliminating index are used as indexes for evaluating the phlegm eliminating activity effect, and the expression quantity of serum inflammatory factors is used as an evaluation index for wide anti-inflammatory.
(3) Experimental results
As shown in the sputum excretion amount measurement results of the mice in fig. 6, compared with CMC-Na (0.23±0.05) μg/mL, AM (1.79±0.26) μg/mL, HSD-H (1.92±0.15) μg/mL, HSD-M (1.37±0.13) μg/mL, the sputum excretion indexes are 678.02% (< 0.0001) and 733.59% (< 0.0001) and 497.52% (< 0.0001) respectively, which have statistical significance, and AM and HSD-H, HSD-M significantly increase the sputum excretion amount of the mice; HSD-L (0.39.+ -. 0.06) μg/mL had an expectorant index of 70.48% (ns), no significant difference from CMC-Na.
As shown in the TNF- α measurement results of mouse serum in fig. 7, compared with CMC-Na (344.56 ±30.15) pg/mL, AM (98.19±19.40) pg/mL, HSD-H (102.59 ±17.65) pg/mL, HSD-M (163.56 ±10.97) pg/mL, HSD-L (250.59 ±12.96) pg/mL, the content of anti-inflammatory factor TNF- α in serum is reduced by 71.50% (P < 0.001), 70.23% (P < 0.001), 52.53% (P < 0.05), 27.27% (ns), respectively, and AM and HSD-H, HSD-M significantly reduce the content of TNF- α in serum, which is statistically significant; HSD-L was not significantly different from CMC-Na.
As shown in the measurement results of IL-1β in mice in FIG. 8, compared with CMC-Na (404.58 + -8.88) pg/mL, AM (188.87 + -7.47) pg/mL, HSD-H (212.74 + -16.10) pg/mL, HSD-M (214.74 + -15.16) pg/mL, HSD-L (332.38 + -14.46) pg/mL, the content of anti-inflammatory factor IL-1β in serum is reduced by 53.32% (P < 0.001), 47.42% (P < 0.01), 47.05% (P < 0.01), 17.85% (ns), and AM and HSD-H, HSD-M significantly reduce the content of IL-1β in serum, respectively, which has no significance in statistics.
Experimental example 3: anti-inflammatory experiment
(1) Grouping and administration of animals
30 SPF-class 4-week-old ICR male mice were obtained and supplied from the university of Zhongshan (the center of laboratory animals, east campus), and the laboratory animals were given license numbers: SCXK (Yue) 2021-0029. ICR mice were divided into 5 groups, namely, HSD-L, HSD-M, HSD-H, positive drug control group (dexamethasone, DEXA) and negative control group (CMC-Na), and the doses of the HSD-L, HSD-M, HSD-H administered were 10mg/kg, 20mg/kg and 40mg/kg, respectively, and the positive control group was administered with Dexamethasone (DEXA) 10mg/kg, and the negative drug control group was administered with 0.5% sodium carboxymethyl cellulose (CMC-Na). All drugs were first dissolved in 0.5% sodium carboxymethyl cellulose solution and diluted to the desired concentration depending on the dose. The administration mode is gastric lavage administration.
(2) Model creation and evaluation
The preparation method comprises the following steps of adapting to the environment for 3 days, performing gastric lavage for 7 days, performing no water control after 12 hours of fasted administration in the last day, and applying 10 mu L of dimethylbenzene on the front side and the rear side of the right ear of a mouse after 0.5 hour of administration in the last day, wherein the left ear is used as a control. After 0.5h, the eyeballs were harvested for blood, and sacrificed after neck removal. The ears of the mice are cut off along the auricle baseline, and the ears are punched by a 6mm ear puncher, and the weight of the ears is weighed. And centrifuging the blood after standing to obtain serum, and detecting the expression level of blood inflammatory factors. The ear swelling degree and the inflammation inhibition rate are used as evaluation indexes of anti-inflammatory drug effects, and the expression quantity of serum inflammatory factors is used as an evaluation index of wide anti-inflammatory effect.
(3) Experimental results
As shown in fig. 9, the ear swelling degree was measured, and compared with CMC-Na (88.80 ±13.85)%, DEXA (47.84 ±5.14)%, HSD-H (32.87±2.96)%, HSD-M (49.78 ±5.06)%, and ear swelling degrees were respectively reduced by 46.13% (< 0.01), 62.99% (< 0.001) and 43.95% (< 0.01), and DEXA and HSD-H, HSD-M significantly reduced the ear swelling degree of mice. HSD-L (69.91 + -7.15)%, ear swelling degree was reduced by 21.28% (ns), and there was no significant difference.
As shown in the measurement results of TNF- α in mouse serum of fig. 10, the content of anti-inflammatory factor TNF- α in serum was reduced by 73.13% (< 0.0001), 70.00% (< 0.0001), 60.43% (< 0.0001), 34.06% (< 0.05) compared with CMC-Na (202.19 ±29.96) pg/mL, HSD-H (60.67 ±2.60) pg/mL, HSD-M (80.00±6.79) pg/mL, and DEXA and HSD significantly reduced the content of TNF- α in serum, respectively, which is statistically significant.
As shown in the results of the IL-1β measurement of mouse serum in FIG. 11, compared with CMC-Na (172.00 + -20.39) pg/mL, DEXA (76.96+ -1.00) pg/mL, HSD-H (105.30 + -4.19) pg/mL, HSD-M (123.78 + -4.25) pg/mL, HSD-L (147.35 + -2.28) pg/mL, the content of anti-inflammatory factor IL-1β in serum was reduced by 55.26% (P < 0.001), 38.78% (P < 0.05), 28.03% (ns), 14.33% (ns), DEXA and HSD-H significantly reduced the content of IL-1β in serum, respectively, with no significant difference from CMC-Na.
Finally, it should be noted that the above embodiments are only for illustrating the technical solution of the present invention, and not for limiting the scope of the present invention, and although the present invention has been described in detail with reference to the preferred embodiments, it should be understood by those skilled in the art that modifications or equivalent substitutions can be made to the technical solution of the present invention without departing from the spirit and scope of the technical solution of the present invention.
Claims (7)
1. Application of hesperidin in preparing medicine for treating chronic obstructive pulmonary disease is provided.
2. The use according to claim 1, wherein the medicament comprises hesperidin and one or more pharmaceutically acceptable auxiliaries.
3. The use according to claim 2, wherein the amount of hesperidin in the medicament is 1-100 mg/kg.
4. The use according to claim 3, wherein the amount of hesperidin in the medicament is 5-90mg/kg.
5. The use according to claim 3, wherein the amount of hesperidin in the medicament is 10-40 mg/kg.
6. Use according to claim 3, wherein the auxiliary material comprises: starch, soluble starch, microcrystalline cellulose, magnesium stearate, lactose, dextrin, sodium hydroxymethyl cellulose, and pulvis Talci.
7. The use according to claim 1, wherein the medicament is in the form of a tablet, capsule, granule, powder, oral liquid, granule, pill.
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Citations (5)
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| US20120121730A1 (en) * | 2010-10-07 | 2012-05-17 | Trinity Laboratories, Inc. | Pharmaceutical and nutraceutical compositions for treating respiratory disease and associated phlegm |
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| CN103417563A (en) * | 2013-08-08 | 2013-12-04 | 中国科学院广州生物医药与健康研究院 | Application of aurantiamarin to preparation of medicine for treating acute and chronic bronchitis |
| CN107582585A (en) * | 2017-11-08 | 2018-01-16 | 河南中医药大学 | Treat traditional Chinese medicinal components side and its application of COPD syndrome of qi deficiency of lung and kidney |
| WO2021248254A2 (en) * | 2020-10-09 | 2021-12-16 | Ingenew Pharma Inc. | Pharmacotherapeutic doses of hesperidin or related bioflavonoids to adress infectious and/or inflammatory diseases |
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| US20120121730A1 (en) * | 2010-10-07 | 2012-05-17 | Trinity Laboratories, Inc. | Pharmaceutical and nutraceutical compositions for treating respiratory disease and associated phlegm |
| CN102526181A (en) * | 2011-12-31 | 2012-07-04 | 吉林草还丹药业有限公司 | Pharmaceutical composition for relieving cough and eliminating phlegm |
| CN103417563A (en) * | 2013-08-08 | 2013-12-04 | 中国科学院广州生物医药与健康研究院 | Application of aurantiamarin to preparation of medicine for treating acute and chronic bronchitis |
| CN107582585A (en) * | 2017-11-08 | 2018-01-16 | 河南中医药大学 | Treat traditional Chinese medicinal components side and its application of COPD syndrome of qi deficiency of lung and kidney |
| WO2021248254A2 (en) * | 2020-10-09 | 2021-12-16 | Ingenew Pharma Inc. | Pharmacotherapeutic doses of hesperidin or related bioflavonoids to adress infectious and/or inflammatory diseases |
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