천식은 기도에 염증을 일으키고 협착시키는 만성 폐질환 입니다.
천식은 반복적 천명음 (호흡할 때 휘파람 소리가 들림), 흉부 압박감, 호흡 곤란, 기침을 일으킵니다.
기침은 종종 밤이나 이른 아침에 발생합니다.
Asthma is a chronic lung disease that inflames and narrows the airways. Asthma
causes recurring periods of wheezing (a whistling sound when you breathe),
chest tightness, shortness of breath, and coughing. The coughing often occurs
at night or early in the morning.
천식은 모든 연령층 사람들이 걸리지만 대부분은 어린 시절부터 시작됩니다.
미국에서는
2500만 명이 천식이 있는 것으로 알려져 있습니다.
이들 중 약 7백만 명이 어린이입니다.
Asthma affects people of all ages, but it most often starts during childhood.
In the United States, more than 25 million people are known to have asthma.
About 7 million of these people are children.
천식을 이해하려면 기도가 작용하는 방식을 아는 것이 도움이 됩니다.
기도는 폐 안팎으로 공기를 운반하는 튜브입니다.
천식 환자는기도에 염증이 있습니다.
염증으로 인해 기도가 부어 오르고 매우 민감해집니다. 기도는 특정 흡입물질에 강하게 반응하는 경향이 있습니다.
CBD 햄프오일 전문
www.dopzamall.com
To understand asthma, it helps to know how the airways work.
The airways are tubes that carry air into and out of your lungs.
People who have asthma have inflamed airways. The inflammation makes the
airways swollen and very sensitive.
The airways tend to react strongly to certain inhaled substances.
기도가 반응하면 주위의 근육이 조여집니다.
이것이 기도를 좁히고, 더 적은 공기가 폐로 흐르게 합니다.
부기도 악화되어 기도가 더 좁아질 수 있습니다.
기도에 있는 세포는 평소보다 더 많은 점액을 만들 수 있습니다.
점액은 끈적거리고 두꺼운 액체로기도를 더 좁힐 수 있습니다.
When the airways react, the muscles around them tighten. This narrows the
airways, causing less air to flow into the lungs. The swelling also can worsen,
making the airways even narrower. Cells in the airways might make more
mucus than usual. Mucus is a sticky, thick liquid that can further narrow the
airways.
이 연쇄 반응은 천식 증상을 일으킬 수 있습니다. 증상은 기도에 염증이 생길 때마다 발생할 수 있습니다.
This chain reaction can result in asthma symptoms. Symptoms can happen each
time the airways are inflamed.
국립 심장, 혈액 및 폐 연구소
National Heart, Blood and Lung Institute
아래는 천식에 대한 칸나비스 연구 라이브러리입니다.
Below is a Library of Cannabis Research Studies for Asthma.
천식의
Murine 모델에서
알레르기 기도 염증을 제한하는 천연 살해 세포를 조절하는 CB2 수용체
CB2 Receptors Regulate Natural Killer Cells that Limit Allergic Airway
Inflammation in a Murine Model of Asthma
2016년 12월
개요
Abstract
"알레르기성
천식은 타고난 면역 반응과 적응 면역반응의 보완작용을 포함하는 만성기도 염증성 질환입니다.
CB2 수용체를 통해 작용하는 체내칸나비노이드는 항상성 및 염증성 과정 모두에서 중요한 역할을 합니다.
그러나,
공통 집먼지 진드기(HDM) 알레르기 항원에 대한 감작 이전의 타고난 사건에 대한 CB2- 작용 에이코사노이드의 기여는 아직 밝혀지지 않았습니다.
알레르기 항원유발 폐염증 및 자연 살해세포 효과기 기능 중 CB2 활성화의 역할을 조사했습니다.
CB2 결핍
(CB2 - / -) 쥐의
폐 점막 반응을 검사하고 야생형(WT) HDM 알레르겐에 대한 비내 노출 ...
CB2 수용체가 결핍된 쥐는 알레르기 항원 흡입후 기도 호산 구성 감소, 2 형 사이토카인 생성과 점액분비감소와 같은 알레르기성 염증유도에 저항성이 있지만 폐 NK 세포 수가 증가했습니다.
이 현상은 WT쥐가 CBM-특이 길항제로 치료되어 HDM-유도기도 염증 및 잔세포증식의 현저한 억제를 유발할 때 확증되었습니다.
CB2 - / - 쥐의
폐에서의
NK 세포의 우세는 2 그룹의 선천성 림프 세포 (ILC2s)의 감소와 유의한 상관관계가 있었습니다.
NK 세포 고갈은 폐에서의 알레르겐 반응성을 회복 시켰으며, ILC2 수치의 상승과 관련이 있었습니다.
이러한 결과는 CB2 활성화가 폐 NK 세포기능을 조절하는데 결정적이고 NK 세포가 ILC2 활성화 및 그 후의 알레르기 기도를 제한하는 역할을 한다는 것을 보여줍니다.
CB2 억제는 폐 염증 동안 NK 세포 반응을 조절하는 중요한 목표를 제시할 수 있습니다.
“Allergic asthma is a chronic airway inflammatory disease involving the
complementary actions of innate and adaptive immune responses. Endogenously
generated cannabinoids acting via CB2 receptors play important roles in both
homeostatic and inflammatory processes. However, the contribution of CB2-acting
eicosanoids to the innate events preceding sensitization to the common house
dust mite (HDM) allergen remains to be elucidated. We investigated the role of
CB2 activation during allergen-induced pulmonary inflammation and natural
killer (NK) cell effector function…Lung mucosal responses in CB2-deficient (CB2−/−)
mice were examined and compared with wild-type (WT) littermates following
intranasal exposure to HDM allergen…Mice
lacking CB2 receptors exhibited elevated numbers of pulmonary NK cells yet were
resistant to the induction of allergic inflammation exemplified by diminished
airway eosinophilia, type 2 cytokine production and mucus secretion after
allergen inhalation. This phenomenon was corroborated when WT mice were treated
with a CB2-specific antagonist that caused a pronounced inhibition of
HDM-induced airway inflammation and goblet cell hyperplasia. Unexpectedly, the
preponderance of NK cells in the lungs of CB2−/−
mice correlated with reduced numbers of group 2 innate lymphoid cells (ILC2s).
Depletion of NK cells restored the allergen responsiveness in the lungs and was
associated with elevated ILC2 numbers…Collectively, these results reveal that
CB2 activation is crucial in regulating pulmonary NK cell function, and suggest
that NK cells serve to limit ILC2 activation and subsequent allergic airway
inflammation. CB2 inhibition may present an important target to modulate NK
cell response during pulmonary inflammation.” — Study
쥐에서의
Dinitrofluorobenzene 유발
실험
천식에
대한
칸나비노이드의
영향
The Effect Of Cannabinoids On Dinitrofluorobenzene-induced Experimental
Asthma In Mice
Respiratory, Physiology, and Neurobiology | September 2016
개요
Abstract
"칸나비노이드는
항 염증 효과가 있으며 기도에서 기관지 확장을 일으킬 수 있습니다.
쥐에서
dinitrofluorobenzene (DNFB)에
의해 유도된 실험적 비 아토피 성 천식에서 기관 내 과민 반응과기도 염증에 대한 칸나비노이드의 영향을 조사했습니다.
carbachol 및
전기장 자극에 의한 수축과 이소프레날린에 의한 이완 반응은 DNFB 군에서 변함없이 유지되는 반면, 5- 하이드 록시트립타민 (5-HT)에 의한 수축 반응은 증가되었습니다.
증가된
5-HT- 유도
수축은 아트로핀 또는 테트로도톡신과의 항온 처리에 의해 억제되었습니다.
DNFB 적용은 기관지 폐포 세척액 (BALF)에서 증가된 대식세포 수를 초래했습니다.
생체 내 ACEA (CB1 agonist) 치료는 5-HT 수축의 증가를 막았고, JWH133 (CB2 agonist)는 효과가 없었습니다.
그러나
ACEA 나 JWH133은 BALF에서 대식세포 수의 증가를 막지 못했습니다.
시험관내
ACEA 배양은 또한 DNFB 군에서 5-HT 수축의 증가를 억제했습니다.
이러한 결과는 칸나비노이드 CB1 수용체 작용제가 쥐의 DNFB 유발 비 아토피 천식에서 기관 내 과민반응을 5-HT로 예방할 수 있음을 보여줍니다.
“Cannabinoids have anti-inflammatory effects and can produce bronchodilation in
the airways. We have investigated the effects of cannabinoids on tracheal
hyperreactivity and airway inflammation in dinitrofluorobenzene (DNFB)-induced
experimental non-atopic asthma in mice. 5-hydroxytryptamine (5-HT)-induced
contraction response was enhanced while carbachol- and electrical field
stimulation-induced contractions, and isoprenaline-induced relaxation responses
were remained unchanged in DNFB group. The increased 5-HT-induced contractions
were inhibited by incubation with either atropine or tetrodotoxin. DNFB
application resulted in increased macrophage number in the bronchoalveolar
lavage fluid (BALF). In vivo ACEA (CB1 agonist) treatment prevented the increase
in 5-HT contractions, while JWH133 (CB2 agonist) had no effect. However,
neither ACEA nor JWH133 prevented the increase in macrophage number in BALF. In
vitro ACEA incubation also inhibited the increase in 5-HT contraction in DNFB
group. These results show that cannabinoid CB1 receptor agonist can prevent
tracheal hyperreactivity to 5-HT in DNFB-induced non-atopic asthma in mice.” —
Study
Δ9-Tetrahydrocannabinol Reverses TNFα-induced Increase In Airway Epithelial
Cell Permeability Through CB2 Receptors
Biochemical Pharmacology | November 2016
Abstract: “Despite pharmacological treatment, bronchial hyperresponsiveness
continues to deteriorate as airway remodelling persists in airway inflammation.
Previous studies have demonstrated that the phytocannabinoid Δ9-tetrahydrocannabinol
(THC) reverses bronchoconstriction with an anti-inflammatory action. The aim of
this study was to investigate the effects of THC on bronchial epithelial cell
permeability after exposure to the pro-inflammatory cytokine, TNFα.
Calu-3 bronchial epithelial cells were cultured at air-liquid interface.
Changes in epithelial permeability were measured using Transepithelial
Electrical Resistance (TEER), then confirmed with a paracellular permeability
assay and expression of tight junction proteins by Western blotting.
Treatment with THC prevented the TNFα-induced decrease in TEER and increase in
paracellular permeability. Cannabinoid CB1 and CB2 receptor-like
immunoreactivity was found in Calu-3 cells. Subsequent experiments revealed
that pharmacological blockade of CB2, but not CB1 receptor inhibited the THC
effect. Selective stimulation of CB2 receptors displayed a similar effect to
that of THC. TNFα decreased expression of the tight junction proteins occludin
and ZO-1, which was prevented by pre-incubation with THC.
These data indicate that THC prevents cytokine-induced increase in airway
epithelial permeability through CB2 receptor activation. This highlights that
THC, or other cannabinoid receptor ligands, could be beneficial in the prevention
of inflammation-induced changes in airway epithelial cell permeability, an
important feature of airways diseases.” — Study
Evaluation Of Serum Cytokines Levels And The Role Of Cannabidiol Treatment In
Animal Model Of Asthma
Mediators of Inflammation | May 2015
Abstract: “Asthma represents a public health problem and traditionally is
classified as an atopic disease, where the allergen can induce clinical airway
inflammation, bronchial hyperresponsiveness, and reversible obstruction of
airways. Studies have demonstrated the presence of T-helper 2 lymphocytes in
the lung of patients with asthma.These cells are involved in cytokine
production that regulates immunoglobulin synthesis. Recognizing that T cell
interaction with antigens/allergens is key to the development of inflammatory
diseases, the aim of this study is to evaluate the anti-inflammatory potential
of cannabidiol (CBD) in this setting. Asthma was induced in 8-week-old Wistar
rats by ovalbumin (OVA). In the last 2 days of OVA challenge animals received
CBD (5 mg/kg, i.p.) and were killed 24 hours after. The levels of IL-4, IL-5,
IL-13, IL-6, IL-10, and TNF- were determinate in the serum. CBD treatment was
able to decrease the serum levels of all analyzed cytokines except for IL-10
levels. CBD seems to be a potential new drug to modulate inflammatory response
in asthma.” — Study
The Cannabinergic System As A Target For Anti-inflammatory Therapies
Current Topics in Medicinal Chemistry | 2006
Abstract: “Habitual cannabis use has been shown to affect the human immune
system, and recent advances in endocannabinoid research provide a basis for
understanding these immunomodulatory effects. Cell-based experiments or in vivo
animal testing suggest that regulation of the endocannabinoid circuitry can
impact almost every major function associated with the immune system. These
studies were assisted by the development of numerous novel molecules that exert
their biological effects through the endocannabinoid system. Several of these
compounds were tested for their effects on immune function, and the results
suggest therapeutic opportunities for a variety of inflammatory diseases such
as multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, atherosclerosis,
allergic asthma, and autoimmune diabetes through modulation of the
endocannabinoid system.” — Study
Comparison Of Bronchial Effects Of Nabilone And Terbutaline In Healthy And
Asthmatic Subjects
Journal of Clinical Pharmacology | April 1983
Abstract: “The acute bronchomotor effect of nabilone, a synthetic cannabinoid
compound, was compared to that of terbutaline sulfate and placebo in six
healthy and six asthmatic subjects. Bronchodilation following nabilone was
intermediate between that of terbutaline and placebo in the healthy subjects
but was equivalent to placebo in the asthmatics. We conclude that oral nabilone
(2 mg) does not result in significant acute bronchodilation in patients with
asthma.” — Study
Bronchodilator Effect Of Delta1-Tetrahydrocannabinol
British Journal of Clinical Pharmacology | June 1978
Abstract: “1 delta1-trans-tetrahydrocannabinol, (delta1-THC) produces
bronchodilatation in asthmatic patients. 2 Administered in 62 microliter
metered volumes containing 50–200 microgram by inhalation from an aerosol
device to patients judged to be in a steady state, it increased peak expiratory
flow rate (PEFR) and forced expiratory volume in 1 second (FEV1). 3 The rate of
onset, magnitude, and duration of the bronchodilator effect was dose related.”
— Study
Bronchial Effects Of Aerosolized Delta 9-Tetrahydrocannabinol In Healthy And
Asthmatic Subjects
댓글