Galleria mellonella 유충의 Candida albicans 감염에 대한 Cordyceps militaris 추출물의 면역조절 및 보호 효과.

한국어 요약

2024년 발표된 「Immunomodulation and Protective Effects of Cordyceps militaris Extract Against Candida albicans Infection in Galleria mellonella Larvae.」은(는) Cordyceps militaris (동충하초) 및 코디세핀 관련 동물·세포 실험(전임상)입니다. 아래는 원문 초록을 바탕으로 한 중립적 요약이며, 제품 효능·효과를 의미하지 않습니다.

초록 요지

Clinically, osteoarthritis (OA) pain is significantly associated with synovial inflammation. Identification of the mechanisms driving inflammation could reveal new targets to relieve this prevalent pain state. Herein, a role of polyadenylation in OA synovial samples was investigated, and the potential of the polyadenylation inhibitor cordycepin (3' deoxyadenosine) to inhibit inflammation as well as to reduce pain and structural OA progression were studied. Joint tissues from people with OA with high or low grade inflammation and non-arthritic post-mortem controls were analysed for the polyadenylation factor CPSF4 and inflammatory markers. Effects of cordycepin on pain behavior and joint pathology were studied in models of OA (intra-articular injection of monosodium iodoacetate in rats and surgical destabilisation of the medial meniscus in mice). Human monocyte-derived macrophages and a mouse macrophage cell line were used to determine effects of cordycepin on nuclear localisation of the inflammatory transcription factor NFĸB and polyadenylation factors (WDR33 and CPSF4). CPSF4 and NFκB expression were increased in synovia from OA patients with high grade inflammation. Cordycepin reduced pain behaviour, synovial inflammation and joint pathology in both OA models. Stimulation of macrophages induced nuclear localisation of NFĸB and polyadenylation factors, effects inhibited by cordycepin. Knockdown of polyadenylation factors also prevented nuclear localisation of NFĸB. The increased expression of polyadenylation factors in OA synovia indicates a new target for analgesia treatments. This is supported by the finding that polyadenylation factors are required for inflammation in macrophages and by the fact that the polyadenylation inhibitor cordycepin attenuates pain and pathology in models of OA.

전문가 메모

• 연구 수준: 동물/세포 실험 · 동물·세포 실험(전임상)
• 대상: Cordyceps militaris (동충하초) / cordycepin
• 제품 연관성: direct
• 해석 주의: 전임상(동물·세포) 결과는 인간 섭취·담금주 맥락으로 직접 확장하기 어렵습니다.
• 해석 주의: 원문에 질병·치료 관련 서술이 포함되어 있습니다. 본 요약은 성분·균류 연구 맥락만 중립적으로 정리했습니다.
• 인사이트: 배양·생산·기초 메커니즘 연구로 읽는 것이 적절합니다. 소비자 효능 주장 근거로 사용할 수 없습니다.

출처 · 원문

• 제목: Immunomodulation and Protective Effects of Cordyceps militaris Extract Against Candida albicans Infection in Galleria mellonella Larvae.
• 저자: Sadaf Ashraf 외 9명
• 연도: 2024
• 저널: Insects
• DOI: 10.1038/s41598-019-41140-1
• PMID: 39590481
• 링크: https://pubmed.ncbi.nlm.nih.gov/39590481/

원문 초록 (English)

Summary — Clinically, osteoarthritis (OA) pain is significantly associated with synovial inflammation. Identification of the mechanisms driving inflammation could reveal new targets to relieve this prevalent pain state. Herein, a role of polyadenylation in OA synovial samples was investigated, and the potential of the polyadenylation inhibitor cordycepin (3' deoxyadenosine) to inhibit inflammation as well as to reduce pain and structural OA progression were studied. Joint tissues from people with OA with high or low grade inflammation and non-arthritic post-mortem controls were analysed for the polyadenylation factor CPSF4 and inflammatory markers. Effects of cordycepin on pain behavior and joint pathology were studied in models of OA (intra-articular injection of monosodium iodoacetate in rats and surgical destabilisation of the medial meniscus in mice). Human monocyte-derived macrophages and a mouse macrophage cell line were used to determine effects of cordycepin on nuclear localisation of the inflammatory transcription factor NFĸB and polyadenylation factors (WDR33 and CPSF4). CPSF4 and NFκB expression were increased in synovia from OA patients with high grade inflammation. Cordycepin reduced pain behaviour, synovial inflammation and joint pathology in both OA models. Stimulation of macrophages induced nuclear localisation of NFĸB and polyadenylation factors, effects inhibited by cordycepin. Knockdown of polyadenylation factors also prevented nuclear localisation of NFĸB. The increased expression of polyadenylation factors in OA synovia indicates a new target for analgesia treatments. This is supported by the finding that polyadenylation factors are required for inflammation in macrophages and by the fact that the polyadenylation inhibitor cordycepin attenuates pain and pathology in models of OA.

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