CN108635345A - Based on the inflammatory conditions protective agents of blood vessel endothelium inflammatory damage and its application - Google Patents
Based on the inflammatory conditions protective agents of blood vessel endothelium inflammatory damage and its application Download PDFInfo
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Abstract
Inflammatory conditions protective agents based on blood vessel endothelium inflammatory damage, the drug are chlorogenic acid, application of the chlorogenic acid in terms for the treatment of of vascular inflammatory conditions.Chlorogenic acid can the induction of substantially reduced complement bypass-activation chmice acute injury of lungs, mechanism may be with the phosphorylation for inhibiting NF κ B p65 and to reduce inflammatory reaction degree related.
Description
Technical field
The present invention relates to chlorogenic acid application fields, more particularly to the inflammatory conditions prevention based on blood vessel endothelium inflammatory damage
Drug and its application.
Background technology
The occurrence and development of many cardiovascular and cerebrovascular diseases and the damage of vascular endothelial cell are closely related.Endothelial cell
(endothelial cell, EC) not only constitutes the barrier between vascular smooth muscular tissue and blood, but also with adjusting blood
All more important active functions of Physiological effect such as pipe tension, fibrinolytic, anti-freezing, inflammatory reaction.EC is not only many symptom and pathology
Important target organ in damage, but also it is important effector organ.A variety of damages or stimulus can lead to endothelial cell knot
The variation of structure and function, and this variation is once continue will make endothelial cell occur damaging and apoptosis, intravascular to destroy
The integrality of skin causes subsequent inflammation and pathology damage.In acute lung injury, pyemia, ischemical reperfusion injury, burning (wound)
The diseases such as wound, systemic inflammatory response syndrome, autoimmune disease, atherosclerosis, diabetes, multiple organ failure
In the occurrence and development of symptom, activation, damage and the inflammatory effector of EC play important role.
And in many factors for causing EC to damage, complement has important pathological effect.Complement is the weight of immune system
Component part is wanted, is played a significant role in body natural protection, immunoregulation.But the excessive activation of complement can cause inflammation and
The excessive activation of tissue damage, especially complement bypass plays important angle in a series of occurrence and development of diseases and symptom
Color.And complement cause inflammation and tissue damage key be after its activation caused by EC inflammatory reactions.Based on complement bypass
The EC inflammatory reactions that activation causes are the important general character mechanism that many related diseases are levyd in disease.)
Chlorogenic acid, (Chlorogenic acid, hereinafter referred to as CA) are the depsides generated by caffeic acid and chinic acid,
It is a kind of phenylpropanoids that plant generates during aerobic respiration through shikimic acid pathway, is primarily present in gold and silver
In many medicinal materials such as flower, Honeysuckle flower, Cortex Eucommiae；Its product is respectively Honegsukle flower P.E, eucommia ulmoides extracts etc., and chlorogenic acid is considered
It is the principle active component of numerous medicinal materials and Chinese patent drug antibacterial and detoxicating, anti-inflammatory and choleretic, is normally used as qualitative or even quantitative finger
Mark.
Invention content
To solve the above-mentioned problems of the prior art, the purpose of the present invention is to provide based on blood vessel endothelium inflammatory damage
Inflammatory conditions protective agents and its application.
In order to achieve the above objectives, the technical scheme is that：
The inflammatory conditions protective agents based on blood vessel endothelium inflammatory damage, the active constituents of medicine are green original
Acid.
Further, the chlorogenic acid is pill, tablet, injection or capsule.
Further, the application of the inflammatory conditions protective agents based on blood vessel endothelium inflammatory damage is specially：It is green
Application of the ortho acid in treatment of vascular aspect of inflammation.
Compared with the existing technology, beneficial effects of the present invention are：
Chlorogenic acid is medicine common drug, but is not intended as before medically only using chlorogenic acid as detection indicator
Specific medicinal ingredient thinks that it does not occur curative effect, the present invention it has been investigated that, chlorogenic acid has cures base well
In the effect of the inflammatory conditions of blood vessel endothelium inflammatory damage, existing technology prejudice is broken, has been of great significance.
Description of the drawings
Fig. 1 be chlorogenic acid to inflammatory mediator and adhesion molecule in mice with acute lung injury BALF influence (n=8, M ±
SD)；Note：Compared with normal group, #P<0.05, ##P<0.01；Compared with model group, * P<0.05, * * P<0.01
Wherein (A：The concentration of IL-6 in mice with acute lung injury BALF；B：TNF-α is dense in mice with acute lung injury BALF
Degree；C：The concentration of P-selectin in mice with acute lung injury BALF；D：The concentration of ICAM-1 in mice with acute lung injury BALF)
Fig. 2 chlorogenic acids to inflammatory mediator and adhesion molecule in mice with acute lung injury serum influence (n=8, M ±
SD)；Note：Compared with normal group, #P<0.05, ##P<0.01；Compared with model group, * P<0.05, * * P<0.01
Wherein (A：The concentration of IL-6 in mice with acute lung injury serum；B：TNF-α is dense in mice with acute lung injury serum
Degree；C：The concentration of P-selectin, D in mice with acute lung injury serum：The concentration of ICAM-1 in mice with acute lung injury serum)
Fig. 3 pathologics histological observation (× 200), wherein A：Normal group；B：Model group；C：Resveratrol group；D：
Chlorogenic acid group
Influence (× the 200) (n=of Fig. 4 chlorogenic acids to NF- κ B p65 phosphorylation levels in mice with acute lung injury lung tissue
8, M ± SD), wherein Fig. 4 A：The immunohistochemistry testing result of lung tissue, wherein A：Normal group；B：Model group；C：Resveratrol
Group；D：Chlorogenic acid group；
Fig. 4 B：The analysis of NF- κ B p65 phosphorylation levels in lung tissue
Specific implementation mode
Technical solution of the present invention is described in further detail with reference to the accompanying drawings and detailed description：
As shown in Figure 1, experimental example：
Acute lung injury (acute lung injury, ALI) be endanger human health a kind of common clinical it is suddenly critical
Disease, case fatality rate is high, seriously threatens the life of patient and influences its life quality, clinically also lacks having for treatment ALI at present
Effect means.ALI morbidity early stages, complement system are activated first, especially the inflammation of microvascular endothelial cells caused by complement activation
Disease is reacted and damage plays key player in the occurrence and development of ALI.Chlorogenic acid (chlorogenic acid, CGA) is expensive
Typical reactive ingredient in many medicinal materials such as state characteristic Ethnic crude drugs honeysuckle, Honeysuckle flower, Cortex Eucommiae has antibacterial, antiviral, anti-
The effects that scorching.Our early-stage studies find that CGA has human microvascular endothelial cell (mvec) inflammatory reaction caused by complement bypass-activation
Preferable intervention effect, therefore, this experiment use ALI mouse models caused by complement bypass-activation to the protective effect of CGA into
Row research and evaluation.
1, experiment material
KM mouse, half male and half female are purchased from Hunan SJA Laboratory Animal Co. , Ltd, production licence：SCXK-
(Hunan) -2013-0004.Cobra-venom factor (cobra venom factor, CVF) is that this project team system is standby.Chlorogenic acid
(CGA), resveratrol (resveratrol, Res) is purchased from Beijing Suo Laibao Co., Ltds.MPO kits build up life purchased from Nanjing
Object Graduate School of Engineering.Mouse IL-6, TNF-α, P-selectin, ICAM-1ELISA kit are purchased from Wuhan doctor's moral biology work
Journey Co., Ltd.NF- κ B p65 antibody is purchased from Santa Cruz companies.Two sulphur amino first of nuclear factor NF- kB inhibitors pyrrolidines
Sour (PDTC), BCA protein quantification kits are purchased from the green skies biotechnology research institute in Jiangsu.All operations and experiment flow are equal
It abides by《Management of laboratory animal regulations》.Experimental situation：Constant temperature (22 ± 2) DEG C, humidity 60%~70%, free water and feed.
2, experimental method
2.1 modellings and administration materials
SPF grades of KM mouse (25 ± 3g) 32 after adaptable fed 5d, are randomly divided into Normal group, model after weighing
Group, Res 40mg/kg groups, CGA 100mg/kg groups, every group 8.Each group mouse prevention administration 7d, wherein CGA groups are daily through filling
Stomach gives the dosage of 100mg/kg, and Res groups (positive control medicine group) give the dosage of 40mg/kg through gavage daily, in 7d
The CVF (with the PBS dilutions that sterilize) of 25 μ g/kg of 1h tail vein injections, the isometric PBS of Normal group tail vein injection after administration.
Each group mouse prevention administration 7d, the CVF (with the PBS dilutions that sterilize) of 25 μ g/kg of 1h tail vein injections, normal right after 7d administrations
According to the isometric PBS of group tail vein injection.It gives 1h after CVF and plucks eyeball and blood, 3000r/min centrifugations 10min is taken to prepare serum；Then
Mouse is put to death, thoracic cavity is opened and gently provokes right lung, right lung, exposure tracheae, promoting the circulation of qi cannula, left lung 1.2mL are clamped with artery clamp
4 DEG C of physiology salt moisture, 4 progress bronchoalveolar lavages, each 0.3mL, lavation 3 times, obtain BAL fluid back and forth
(BALF) row cell count, 4 DEG C of BALF3000r/min centrifuge 10min after counting, and supernatant is taken to dispense, -80 DEG C freeze it is spare.
Superior lobe of right lung is placed in -80 DEG C to freeze, the middle lobe of right lung claims weight in wet base, inferior lobe of right lung to be placed in 4% paraformaldehyde solution fixed.
2.2 moisture content of lung and MPO are measured
Mouse modeling is drawn materials after weighing, and superior lobe of right lung freezes at once in -80 DEG C after taking out and measured for MPO, specific method
It is carried out according to kit specification.Middle lobe of right lung claims weight in wet base, then with 70 DEG C of baking 48h to constant weight, according to formula：(weight in wet base-is dry
Weight)/weight in wet base × 100%, calculate moisture content of lung.
2.3BALF cell counts and determination of protein concentration
Take BALF liquid, row cell count, the total number of cells n of five big lattice on count plate, by formula：Cell number (a/
ML)=total number of cells n/80 × 400 × 104.BALF supernatants are taken, are detected using BCA methods, is measured and is inhaled in 562nm with microplate reader
Shading value simultaneously calculates albumen concentration in BALF.
The measurement of 2.4 inflammatory mediators and adhesion molecule
BALF supernatants and serum are taken, ELISA method detection is used according to kit specification, is surveyed in 450nm with microplate reader
Determine absorbance value and calculates the content of IL-6, TNF-α, P-selectin and ICAM-1.
2.5 pathologic inspections and immunohistochemistry measure
After lavation, inferior lobe of right lung is taken to be fixed with 4% paraformaldehyde solution, makes routine paraffin wax pathological section, HE dyes
Color, microscopically observation.And make immunohistochemical staining, it is positive anti-to occur brown color or brown particle in karyon or endochylema
It answers, with 5.0 image analyses of IPP, measures Positive area and OD value, calculate average optical density value and counted
Analysis, detection NF- κ B p65 Expression of phosphorylated are horizontal.
2.6 statistical analysis
Experimental result is indicated with means standard deviation (M ± SD), for statistical analysis with SPSS 18.0, using t examine into
Row statistical analysis.The data of Non-Gaussian Distribution compare using nonparametric statistical method.P<0.05 is statistically significant for difference.
3 experimental results
Influences of the 3.1CGA to ALI mouse lung tissue indexs of correlation
Compared with normal group, model group mouse BALF cell numbers and MPO contents significantly increase (P<0.05,0.01).With
Model group compares, and Res, CGA can substantially reduce BALF cell numbers (P<0.05,0.01) MPO contents (P, is reduced<0.01).
Model group protein content is higher than Normal group, and Res, CGA can reduce protein content in mouse BALF after prevention administration, but poor
Different no conspicuousness (P>0.05).Each group mouse moisture content of lung is without significant change (P after administration>0.05), it is shown in Table 1.
Influence (n=8, M ± SD) of 1 chlorogenic acid of table to acute lung injury model mouse lung tissue index of correlation
Table1 Effects of CGA on related lung items of ALI mice (n=8, M ± SD)
Note：Compared with normal group,#P<0.05,##P<0.01；Compared with model group,*P<0.05,**P<0.01。
Influences of the 3.2CGA to inflammatory mediator and adhesion molecule in ALI mouse BALF
CGA groups can be such that inflammatory mediator IL-6 in mouse BALF, TNF-α content reduces, and have system with model group comparing difference
Meter learns meaning (P<0.05,0.01), P-selectin and ICAM-1 contents reduce but difference does not have statistical significance (P>
0.05).See influence (n=8, M ± SD) of Fig. 1 chlorogenic acids to inflammatory mediator and adhesion molecule in mice with acute lung injury BALF；
Note：Compared with normal group, #P<0.05, ##P<0.01；Compared with model group, * P<0.05, * * P<0.01
Wherein (A：The concentration of IL-6 in mice with acute lung injury BALF；B：TNF-α is dense in mice with acute lung injury BALF
Degree；C：The concentration of P-selectin in mice with acute lung injury BALF；D：ICAM-1's is dense in mice with acute lung injury BALF
Degree).
Influences of the 3.3CGA to inflammatory mediator and adhesion molecule in ALI mice serums
Compared with normal group, the inflammatory mediator IL-6, TNF-α in model group mice serum and adhesion molecule P-
Selectin, ICAM-1 content dramatically increase (P<0.05,0.01).Compared with model group, Res, CGA group can make in mice serum
IL-6, TNF-α and P-selectin, ICAM-1 content significantly reduce, and difference has statistical significance (P<0.05), see Fig. 2.
Chlorogenic acid is to the influence (n=8, M ± SD) to inflammatory mediator and adhesion molecule in mice with acute lung injury serum；Note：With it is normal
Group compares, #P<0.05, ##P<0.01；Compared with model group, * P<0.05, * * P<0.01
Wherein (A：The concentration of IL-6 in mice with acute lung injury serum；B：TNF-α is dense in mice with acute lung injury serum
Degree；C：The concentration of P-selectin, D in mice with acute lung injury serum：The concentration of ICAM-1 in mice with acute lung injury serum)
3.4 pathologic examination
Pathological section the results show that normally group lung tissue structure it is normal, rare inflammatory cell infiltration；Between the visible lung of model group
Matter is broadening, and alveolar is slightly expanded, universal visible inflammatory cell infiltration；Res and CGA group inflammatory cell infiltrations are substantially reduced, such as scheme
3：Pathologic histological observation (× 200), wherein A：Normal group；B：Model group；C：Resveratrol group；D：Chlorogenic acid group
Influences of the 3.5CGA to ALI mouse NF- κ B p65 phosphorylation levels
Showed by immune group result, compared with normal group, the phosphorylation level of NF- κ Bp65 in model group mouse lung tissue
Significantly increase (P<0.01)；CGA, Res can significantly reduce the phosphorylation level (P of NF- κ B p65 in lung tissue<0.05).See
Fig. 4 A and Fig. 4 B：Wherein, Fig. 4 A：The immunohistochemistry testing result of lung tissue, wherein A：Normal group；B：Model group；C：White black false hellebore
Alcohol group；D：Chlorogenic acid group；
Fig. 4 B：The analysis of NF- κ B p65 phosphorylation levels in lung tissue
4 discussion and conclusion
ALI is with lung's capilary inflammatory reaction and to damage as major pathologic features, thin by inflammation medium and effect
A kind of common Severe acute disease of clinic that born of the same parents participate in jointly.The basic reason of ALI morbidities is the inflammatory reaction that intrapulmonary is excessive, out of control,
Complement plays key player wherein.Complement is the important component of body immune system, the excessive activation of complement system,
Neutrophil leucocyte and mononuclear phagocyte system can be stimulated, by the activation of NF- κ B signal conduction paths, induce a large amount of cells because
The generation of son, inflammatory mediator and protease, causes the runaway inflammatory reaction of acute stage lung.Seminar's early-stage study finds CGA
There is preferable intervention effect to human microvascular endothelial cell (mvec) inflammatory reaction caused by complement bypass-activation, therefore, we use
The intervention effects of the ALI mouse models evaluation CGA of the complement bypass-activation induction of seminar's structure early period in vivo, it is right to observe its
The anti-inflammatory and protective effect of ALI.
This experimental studies results shows that continuous gavage is after 1 week, CGA can substantially reduced mouse lung tissue inflammatory infiltration, reduce
Neutrophil leucocyte intrapulmonary assemble, reduce BAL fluid in total number of cells, inflammatory mediator IL-6, TNF-α content and
The concentration of proinflammatory factor IL-6 in serum, TNF-α and adhesion molecule P-selectin, ICAM-1 mitigate NF- κ B p65 phosphorylations
It is horizontal.CGA is polyphenol compound, is the Typical reactive ingredient of many Chinese medicines such as honeysuckle, Honeysuckle flower, Cortex Eucommiae etc., has
Various biological activity.The above result shows that CGA can effectively inhibit the acute inflammatory phases of ALI early stages, mechanism may be with
Inhibit the inflammation associated signal paths that NF- κ Bp65 are mediated to reduce inflammatory reaction correlation.
The study show that CGA has preferable intervention effect to ALI acute inflammatory reactions caused by complement bypass-activation.
This research is not only that the further investigation for the pharmacological effect Function and its mechanisms for further excavating CGA provides valuable thinking,
Prompt CGA that there is good potential applicability in clinical practice simultaneously.
Experimental example 2
In acute lung injury, pyemia, ischemical reperfusion injury, burning (wound) wound, systemic inflammatory response syndrome, diabetes
Etc. in diseases, complement bypass-activation leads to that endothelial cell is inflamed reaction and damage is that above-mentioned many related diseases are levyd in disease
Important general character mechanism, in the experimental result of this case, chlorogenic acid can effectively inhibit the chmice acute that complement bypass-activation induces
Injury of lungs, the index measured from lung's sample and Peripheral Blood sample clearly reflect that chlorogenic acid can effectively inhibit to mend
The activation of the inflammatory reaction of vascular endothelial cell and inflammatory cell caused by body alternative activation, based on above-mentioned other symptom with it is acute
For injury of lungs in the general character pathologic basis of above-mentioned aspect, chlorogenic acid can be equally used for the prevention of these related symptom.
The above description is merely a specific embodiment, but scope of protection of the present invention is not limited thereto, any
The change or replacement expected without creative work, should be covered by the protection scope of the present invention.Therefore, of the invention
Protection domain should be determined by the scope of protection defined in the claims.
Claims (3)
1. the inflammatory conditions protective agents based on blood vessel endothelium inflammatory damage, which is characterized in that the active constituents of medicine is
Chlorogenic acid.
2. the inflammatory conditions protective agents according to claim 1 based on blood vessel endothelium inflammatory damage, which is characterized in that
The chlorogenic acid is pill, tablet, injection or capsule.
3. the application of the inflammatory conditions protective agents based on blood vessel endothelium inflammatory damage according to claim 1, specially：
Application of the chlorogenic acid in treatment of vascular aspect of inflammation.
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Cited By (2)
| Publication number | Priority date | Publication date | Assignee | Title |
|---|---|---|---|---|
| CN110787156A (en) * | 2018-08-03 | 2020-02-14 | 华南理工大学 | Application of caffeic acid or chlorogenic acid in preparing AGEs (advanced glycation end products) -induced inflammatory reaction inhibitor |
| CN115554286A (en) * | 2022-11-17 | 2023-01-03 | 云南养瑞科技集团有限公司 | Application of caffeic acid derivative in preparation of medicine for treating chronic obstructive pulmonary disease |
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| CN105902525A (en) * | 2016-04-21 | 2016-08-31 | 北京师范大学 | Application of chlorogenic acid nano powder inhalation in medicine for treating acute lung injury |
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| CN105902525A (en) * | 2016-04-21 | 2016-08-31 | 北京师范大学 | Application of chlorogenic acid nano powder inhalation in medicine for treating acute lung injury |
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| TIAN-YIN LIU等: "Sarcandra glabra combined with lycopene protect rats from lipopolysaccharide induced acute lung injury via reducing inflammatory response", 《BIOMEDICINE & PHARMACOTHERAPY》 * |
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| Publication number | Priority date | Publication date | Assignee | Title |
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| CN110787156A (en) * | 2018-08-03 | 2020-02-14 | 华南理工大学 | Application of caffeic acid or chlorogenic acid in preparing AGEs (advanced glycation end products) -induced inflammatory reaction inhibitor |
| CN115554286A (en) * | 2022-11-17 | 2023-01-03 | 云南养瑞科技集团有限公司 | Application of caffeic acid derivative in preparation of medicine for treating chronic obstructive pulmonary disease |
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Application publication date: 20181012 |