감초의 치주염 잇몸질환 감소효과
감초는 진지발리스(P. gingivalis) 독소를
방어하기 위해 대식세포들이 만드는 사이토카인의 양을 줄여줍니다.(Bodet, La et al. 2008) 염증반응을 완화시켜 줄 수 있다는 얘기입니다.
감초는 또다른 치주염 세균인 AA( Aggregatibacter
actinomycetemcomitans) 독소를 방어하기 위해 우리 몸의 면역세포들이 만드는 단백질 분해효소(MMP)의 양도 줄여줍니다.(La, Tanabe et al. 2011) 치주염의 특징인 잇몸뼈(치조골흡수)
를 방어할 수 있다는 얘기입니다.
실제 동물실험에서 감초는, 진지발리스에 의해
초래되는 잇몸뼈 흡수를 예방하고 치료할 수 있음을 보여줍니다.(Sasaki, Suzuki et al. 2010, Zhu, Wei et al. 2012) 염증에
의해 뼈가 흡수되었다가, 감초를 예방적, 치료용으로 투여한
결과 훨씬 더 정도가 좋아집니다.
또다른 동물실험에서 감초는 진지발리스에 의해 혈관이 확장되고 혈관의 투과성이 증가하는 것도
줄여주는 효과를 보입니다.(Kim, Jeon et al. 2013) 혈관이 확장되고 투과성이 증가하는 것은 염증의 전형적인 현상인데, 이를
줄여줄 수 있다는 겁니다.
실제 환자들을 대상으로한 임상실험에서도 감초는, 보통
잇몸병을 치료하기 위해 처방되는 독시사이클린(Doxycycline) 에 맞먹는 골흡수효소(MMP) 의 감소효과를 보입니다. (Farhad,
Aminzadeh et al. 2013)매우 인상적입니다.
환자들을 대상으로한 또다른 비교연구에서도, 감초는
잇몸에서 피가 나거나 골흡수정도에서 좋은 효과를 보여줍니다.(Madan,
Kashyap et al. 2019)
Bodet, C., et al.
(2008). "A licorice extract reduces lipopolysaccharide‐induced proinflammatory cytokine secretion by macrophages and whole
blood." 79(9): 1752-1761.
Farhad, S. Z., et al. (2013).
"The effect of adjunctive low-dose doxycycline and licorice therapy on
gingival crevicular fluid matrix metalloproteinase-8 levels in chronic
periodontitis." Dental research journal 10(5): 624-629.
study compared the effect of adjunctive low dose doxycycline and licorice on
gingival crevicular fluid (GCF) matrix metalloproteinase-8 (MMP-8) levels in
patients with chronic periodontitis. MATERIALS AND METHODS: In this in vivo,
experimental study 39 patients with mild to moderate chronic periodontitis were
selected. Samples of GCF were collected from three deepest pockets and MMP-8
concentration was measured. Patients were divided into three groups (n = 13).
Groups were treated with doxycycline, licorice and placebo. Sampling and
measurement of MMP-8 was repeated after 6 weeks. Data was analyzed by t-paired
and ANOVA test. P > 0.001 was considered significant. RESULTS: The decrease
in mean of MMP-8 concentration was higher in doxycycline and licorice group in comparison
with the placebo group and the difference was statistically significant (P
value > 0.001). The decrease in mean of MMP-8 concentration was higher in
licorice group than doxycycline group, but the difference was not statistically
significant. CONCLUSION: The present study showed that licorice extract can
prevent the production of MMPs by host cells and can be as useful as
antibiotics like doxycycline to cure periodontal and other inflammatory
diseases. It must be added that no side-effects were observed in usage of
Kim, S.-R., et al. (2013).
"Glycyrrhetinic acid inhibits Porphyromonas gingivalis
lipopolysaccharide-induced vascular permeability via the suppression of
interleukin-8." Inflammation Research 62(2): 145-154.
is a major periodontopathogen that plays a role in the pathogenesis of
periodontal disease. In this study, we investigated the effect of
18alpha-glycyrrhetinic acid (18α-GA), a natural triterpenoid compound derived
from licorice root extract, on P. gingivalis lipopolysaccharide (LPS)-induced
vascular permeability, which is a hallmark of inflammatory diseases such as
La, V. D., et al. (2011).
"Modulation of matrix metalloproteinase and cytokine production by
licorice isolates licoricidin and licorisoflavan A: potential therapeutic
approach for periodontitis." 82(1): 122-128.
Madan, S., et al. (2019).
"Glycyrrhiza glabra: An efficient medicinal plant for control of
periodontitis–A randomized clinical trial." 11(1):
Sasaki, H., et al. (2010).
"18β-glycyrrhetinic acid inhibits periodontitis via
glucocorticoid-independent nuclear factor-κB inactivation in
interleukin-10-deficient mice." Journal of periodontal research 45(6): 757-763.
OBJECTIVE: 18β-Glycyrrhetinic acid (GA) is a natural anti-inflammatory compound
derived from licorice root extract (Glycyrrhiza glabra). The effect of GA on
experimental periodontitis and its mechanism of action were determined in the
present study. MATERIAL AND METHODS: Periodontitis was induced by oral
infection with Porphyromonas gingivalis W83 in interleukin-10-deficient mice.
The effect of GA, which was delivered by subcutaneous injections in either
prophylactic or therapeutic regimens, on alveolar bone loss and gingival gene expressions
was determined on day 42 after initial infection. The effect of GA on
lipopolysaccharide (LPS)-stimulated macrophages, T cell proliferation and
osteoclastogenesis was also examined in vitro. RESULTS: 18β-Glycyrrhetinic acid
administered either prophylactically or therapeutically resulted in a dramatic
reduction of infection-induced bone loss in interleukin-10-deficient mice,
which are highly disease susceptible. Although GA has been reported to exert
its anti-inflammatory activity via downregulation of 11β-hydroxysteroid
dehydrogenase-2 (HSD2), which converts active glucocorticoids to their inactive
forms, GA did not reduce HSD2 gene expression in gingival tissue. Rather, in
glucocorticoid-free conditions, GA potently inhibited LPS-stimulated proinflammatory
cytokine production and RANKL-stimulated osteoclastogenesis, both of which are
dependent on nuclear factor-κB. Furthermore, GA suppressed LPS- and
RANKL-stimulated phosphorylation of nuclear factor-κB p105 in vitro.
CONCLUSION: These findings indicate that GA inhibits periodontitis by
inactivation of nuclear factor-κB in an interleukin-10- and
Zhu, L., et al. (2012).
"Licorice isoliquiritigenin suppresses RANKL-induced osteoclastogenesis in
vitro and prevents inflammatory bone loss in vivo." The International
Journal of Biochemistry & Cell Biology 44(7): 1139-1152.
bone-specialized multinucleated cells, are responsible for bone destructive
diseases such as osteoporosis, periodontitis, and rheumatoid arthritis. Natural
plant-derived products have received substantial attention given their
potential therapeutic and preventive activities against human diseases. In the
present study, we investigated the effects of isoliquiritigenin (ISL), a
natural flavonoid isolated from licorice, on receptor activator of nuclear
factor-κB ligand (RANKL)-induced in vitro osteoclastogenesis and
inflammation-mediated bone destruction in vivo. We observed that ISL
dose-dependently inhibited RANKL-induced osteoclast formation from RAW 264.7
and primary mouse bone marrow-derived macrophages (BMMs), as well as decreased
the extent of lacunar resorption. Specifically, ISL targeted RANKL-induced
osteoclastogenesis and F-actin rings formation at an early stage. The
RANKL-stimulated mRNA expression of osteoclast-related genes and transcription
factors were also diminished by ISL. Mechanistically, ISL blocked the
RANKL-triggered RANK–TRAF6 association, phosphorylation of mitogen-activated
protein kinases (MAPKs), inhibitor of κBα (IκBα) phosphorylation and
degradation, nuclear factor-κB (NF-κB) p65 nuclear translocation, as well as
activator protein (AP)-1 activation. ISL almost abrogated the nuclear factor of
activated T cells (NFATc1) expression and inhibited its nuclear translocation
specifically in pre-osteoclasts. Furthermore, the ectopic introduction of
NFATc1 into osteoclast precursors almost reversed the ISL-elicited
anti-osteoclastogenic effects. Consistent with the in vitro results,
administration of ISL prevented inflammatory bone loss in mice by attenuating
osteoclast activity. Taken together, our results demonstrated that ISL
suppresses RANKL-induced osteoclastogenesis and inflammatory bone loss via
RANK–TRAF6, MAPK, IκBα/NF-κB, and AP-1 signaling pathways. Therefore, ISL may
be considered as a novel therapeutic and/or preventive strategy against lytic