건강한 원료이야기..감초에 대한 연구들 > 공지사항

본문 바로가기

쇼핑몰 검색

회원메뉴

오늘 본 상품

없음

공지사항

건강한 원료이야기..감초에 대한 연구들

페이지 정보

작성일 : 2020.12.26 조회수 : 61회

본문

감초의 치주염 잇몸질환 감소효과

 

1.     감초는 진지발리스(P. gingivalis) 독소를 방어하기 위해 대식세포들이 만드는 사이토카인의 양을 줄여줍니다.(Bodet, La et al. 2008)  염증반응을 완화시켜 줄 수 있다는 얘기입니다.

 


f75d6dcd5612dbda2e178074865e9006_1609118638_8193.jpg

 

2.     감초는 또다른 치주염 세균인 AA( Aggregatibacter actinomycetemcomitans) 독소를 방어하기 위해 우리 몸의 면역세포들이 만드는 단백질 분해효소(MMP) 양도 줄여줍니다.(La, Tanabe et al. 2011) 치주염의 특징인 잇몸뼈(치조골흡수) 를 방어할 수 있다는 얘기입니다.


f75d6dcd5612dbda2e178074865e9006_1609118675_9917.jpg


 

3.     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. 



f75d6dcd5612dbda2e178074865e9006_1609118710_3593.jpg
f75d6dcd5612dbda2e178074865e9006_1609118710_414.jpg


 

4.     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.

 


f75d6dcd5612dbda2e178074865e9006_1609118736_0651.jpg


 

 

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.

 

 

f75d6dcd5612dbda2e178074865e9006_1609118755_6881.jpg

 

 

환자들을 대상으로한 또다른 비교연구에서도, 감초는 잇몸에서 피가 나거나 골흡수정도에서 좋은 효과를 보여줍니다.(Madan, Kashyap et al. 2019)


 f75d6dcd5612dbda2e178074865e9006_1609118767_6479.jpg








 

 

Bodet, C., et al. (2008). "A licorice extract reduces lipopolysaccharideinduced 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.

          BACKGROUND: This 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 licorice extract.

 

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.

          Porphyromonas gingivalis 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 periodontitis.

 

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): 32.

         

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.

          BACKGROUND AND 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 glucocorticoid-independent fashion.

 

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.

          Osteoclasts, 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 bone diseases.

 

5.    

 


첨부파일

사이트 정보

사업자정보확인

회사명 : 주식회사 닥스메디대표 : 노미화사업자 등록번호 : 404-86-00297통신판매업신고번호 : 제 2015 - 고양일산서 - 0773호

주소 : 경기 고양시 일산서구 중앙로 1450 사과나무치과병원 1층 닥스메디 스토어Tel : 031-922-2240FAX : 031-365-4597e-mail : docsmedi@docsmedi.kr정보관리책임자명 : 노미화

Copyright © 2020 주식회사 닥스메디 All Rights Reserved.
go top