{"id":7321,"date":"2024-08-06T19:26:38","date_gmt":"2024-08-06T19:26:38","guid":{"rendered":"https:\/\/longchangextracts.com\/?p=7321"},"modified":"2024-08-06T19:26:38","modified_gmt":"2024-08-06T19:26:38","slug":"three-hundred-rods","status":"publish","type":"post","link":"https:\/\/longchangextracts.com\/hu\/three-hundred-rods\/","title":{"rendered":"H\u00e1romsz\u00e1z PI3K\/AKT\/mTOR \u00fatvonalon alapul\u00f3 r\u00fad el\u0151seg\u00edti a lipopoliszacharid induk\u00e1lta autof\u00e1gi\u00e1t \u00e9s g\u00e1tolja a gyullad\u00e1st a RAW264.7 sejtekben"},"content":{"rendered":"

H\u00e1romsz\u00e1z PI3K\/AKT\/mTOR \u00fatvonalon alapul\u00f3 r\u00fad el\u0151seg\u00edti a lipopoliszacharid induk\u00e1lta autof\u00e1gi\u00e1t \u00e9s g\u00e1tolja a gyullad\u00e1st a RAW264.7 sejtekben
\nA lipopoliszacharid (LPS) egy Gram-negat\u00edv bakt\u00e9riumok \u00e1ltal kibocs\u00e1tott endotoxin, amely az emberi szervezetben a Gram-negat\u00edv bakt\u00e9riumfert\u0151z\u00e9sek \u00e1ltal okozott bakteri\u00e1lis toxicit\u00e1s sor\u00e1n az immunrendszer gyullad\u00e1sos v\u00e1laszreakci\u00f3it serkentheti. A makrof\u00e1gok gyakran r\u00e9szt vesznek a gyullad\u00e1sos v\u00e1laszokban \u00e9s a fagocit\u00f3zisban, \u00e9s az LPS-sel kezelt RAW 264.7 makrof\u00e1gvonal az immunsejtek gyullad\u00e1sos v\u00e1laszainak gyakran haszn\u00e1lt sejtmodellje. Az autof\u00e1gia egy olyan katabolikus folyamat, amelyben a citoplazma tartalm\u00e1t az autof\u00e1gosz\u00f3m\u00e1k a lizosz\u00f3m\u00e1kba sz\u00e1ll\u00edtj\u00e1k, ahol a sejtek homeoszt\u00e1zis\u00e1nak fenntart\u00e1sa \u00e9rdek\u00e9ben kiterjedt lebont\u00e1sra ker\u00fcl. Az autof\u00e1gia, mint fontos sejtmechanizmus, r\u00e9szt vesz k\u00fcl\u00f6nb\u00f6z\u0151 betegs\u00e9gek, p\u00e9ld\u00e1ul autoimmun betegs\u00e9gek, gyullad\u00e1sos betegs\u00e9gek \u00e9s daganatok kialakul\u00e1s\u00e1ban \u00e9s fejl\u0151d\u00e9s\u00e9ben. A gyullad\u00e1sos v\u00e1lasz a szervezet sz\u00f6veteinek egyfajta immunv\u00e9delmi funkci\u00f3ja. A m\u00e9rs\u00e9kelt gyullad\u00e1sos v\u00e1lasz seg\u00edt a szervezet k\u00e1rosod\u00e1s\u00e1nak kijav\u00edt\u00e1s\u00e1ban, de a t\u00falzott gyullad\u00e1sos v\u00e1lasz k\u00e1ros reakci\u00f3khoz vezethet a szervezetben, a szervek, sz\u00f6vetek \u00e9s sejtek degener\u00e1ci\u00f3j\u00e1t \u00e9s elhal\u00e1s\u00e1t okozva, \u00e9s ak\u00e1r az \u00e9letet is vesz\u00e9lyeztetve. Sz\u00e1mos tanulm\u00e1ny k\u00e9tir\u00e1ny\u00fa kommunik\u00e1ci\u00f3t tal\u00e1lt az autof\u00e1gia \u00e9s a gyullad\u00e1s k\u00f6z\u00f6tt. A m\u00e9rs\u00e9kelt autof\u00e1gia gyeng\u00edtheti a gyullad\u00e1sos v\u00e1laszt, de a t\u00falzott autof\u00e1gia s\u00falyosb\u00edthatja a gyullad\u00e1sos v\u00e1laszt. T\u00f6bb immunmedi\u00e1tor induk\u00e1lhatja vagy g\u00e1tolhatja az autof\u00e1gi\u00e1t, de a homeoszt\u00e1zis helyre\u00e1ll\u00edt\u00e1sa nagym\u00e9rt\u00e9kben az autof\u00e1gi\u00e1ra t\u00e1maszkodik. Ez\u00e9rt az autof\u00e1gia gyullad\u00e1sra gyakorolt szab\u00e1lyoz\u00e1si mechanizmus\u00e1nak teljes meg\u00e9rt\u00e9se hat\u00e9konyan kezelheti a gyullad\u00e1sos \u00e9s autoimmun betegs\u00e9geket.
\nA h\u00e1romsz\u00e1z p\u00e1lcika a Toddalia asiatica (L.) Lam, a Rutaceae csal\u00e1dba tartoz\u00f3 n\u00f6v\u00e9ny gy\u00f6ker\u00e9b\u0151l sz\u00e1rmazik. A \"Tujia gy\u00f3gy\u00e1szati feljegyz\u00e9sek\" egy\u00e9rtelm\u0171en r\u00f6gz\u00edtik a \"sz\u00e9l \u00e9s nedvess\u00e9g eloszlat\u00e1s\u00e1t, a v\u00e9rkering\u00e9s el\u0151seg\u00edt\u00e9s\u00e9t, az inak ellaz\u00edt\u00e1s\u00e1t, a duzzanat cs\u00f6kkent\u00e9s\u00e9t \u00e9s a f\u00e1jdalom enyh\u00edt\u00e9s\u00e9t\". K\u00e9miai \u00f6sszet\u00e9tel-vizsg\u00e1latok kimutatt\u00e1k, hogy a Sanbai bot f\u0151 k\u00e9miai \u00f6sszetev\u0151i alkaloidok \u00e9s kumarinok. A modern farmakol\u00f3giai kutat\u00e1sok meger\u0151s\u00edtett\u00e9k, hogy a Sanbai bot kivonata reumaellenes, gyullad\u00e1scs\u00f6kkent\u0151, daganatellenes \u00e9s egy\u00e9b hat\u00e1sokkal rendelkezik. El\u0151zetes k\u00eds\u00e9rleti kutat\u00e1saink kimutatt\u00e1k, hogy a Sanbai bot k\u00e9pes blokkolni az autof\u00e1gia \u00e1raml\u00e1s\u00e1t a foszfatidil-inozitol-3-kin\u00e1z\/protein kin\u00e1z B\/mammalian rapamycin target protein (PI3K\/AKT\/mTOR) jel\u00e1tviteli \u00fatvonalon kereszt\u00fcl, ez\u00e1ltal g\u00e1tolja az MH7A fibroblaszt sejtvonal prolifer\u00e1ci\u00f3j\u00e1t \u00e9s apopt\u00f3zist induk\u00e1l. A Toddalia asiatica alkoholos kivonat (TAAE) autof\u00e1gi\u00e1ban bet\u00f6lt\u00f6tt szerepe azonban m\u00e9g kiforratlan. E vizsg\u00e1lat eredm\u00e9nyei azt mutatt\u00e1k, hogy a TAAE koncentr\u00e1ci\u00f3f\u00fcgg\u0151 m\u00f3don v\u00e1ltja ki az autof\u00e1gi\u00e1t. Annak tov\u00e1bbi ellen\u0151rz\u00e9se \u00e9rdek\u00e9ben, hogy a TAAE fontos szerepet j\u00e1tszik-e a RAW 264.7 makrof\u00e1gok autof\u00e1gi\u00e1j\u00e1ban a PI3K\/AKT\/mTOR \u00fatvonalon kereszt\u00fcl, ez a k\u00eds\u00e9rlet LPS stimul\u00e1lt RAW 264.7 sejteket haszn\u00e1lt modellk\u00e9nt, hogy megvizsg\u00e1lja a TAAE hat\u00e1s\u00e1t a RAW 264.7 sejtek autof\u00e1gi\u00e1j\u00e1ra \u00e9s immunfunkci\u00f3j\u00e1ra, \u00e9s felt\u00e1rja a velesz\u00fcletett immunv\u00e1lasz TAAE szab\u00e1lyoz\u00e1s\u00e1nak molekul\u00e1ris mechanizmus\u00e1t.<\/p>\n

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\nA makrof\u00e1gok az emberi szervezet egyik fontos immunsejtje. Az emberi sz\u00f6vetekbe \u00e9s v\u00e9rbe behatol\u00f3 k\u00f3rokoz\u00f3kkal szemben gyorsan k\u00e9pesek stressz\u00e1llapotokat aktiv\u00e1lni, ami gyullad\u00e1sos reakci\u00f3k sorozat\u00e1hoz vezet. Fontos velesz\u00fcletett immunsejtek, amelyek szorosan kapcsol\u00f3dnak a gyullad\u00e1sok kialakul\u00e1s\u00e1hoz \u00e9s fejl\u0151d\u00e9s\u00e9hez. A gyullad\u00e1s egy \u00f6sszetett k\u00f3ros reakci\u00f3, amelyet az immunrendszer k\u00fcl\u00f6nb\u00f6z\u0151 fizikai reakci\u00f3i okoznak, amikor k\u00fcls\u0151 s\u00e9r\u00fcl\u00e9snek vagy fert\u0151z\u00e9snek van kit\u00e9ve. Sz\u00e1mos kr\u00f3nikus betegs\u00e9g, p\u00e9ld\u00e1ul a neurodegenerat\u00edv betegs\u00e9gek, a reumatoid artritisz, az \u00e9relmeszesed\u00e9s stb. patofiziol\u00f3gi\u00e1j\u00e1nak fontos r\u00e9sz\u00e9t k\u00e9pezi. Egy vizsg\u00e1lat meg\u00e1llap\u00edtotta, hogy a TAAE k\u00e9pes g\u00e1tolni a Toll-like receptor 4\/nukle\u00e1ris faktor - \u03ba B (TLR4\/NF - \u03ba B) \u00fatvonalat, ez\u00e1ltal cs\u00f6kkenti a kollag\u00e9n induk\u00e1lta gyullad\u00e1sos citokinek, az interleukin-1 \u03b2 (IL-1 \u03b2) \u00e9s a tumor nekr\u00f3zis faktor - \u03b1 (TNF - \u03b1) expresszi\u00f3j\u00e1t patk\u00e1nyok szin\u00f3vi\u00e1j\u00e1ban (CIA), g\u00e1tolja a reum\u00e1s artritisz szinovitisz\u00e9t, \u00e9s elnyomja a reum\u00e1s artritisz progresszi\u00f3j\u00e1t. A TAAE g\u00e1tolhatja az NF - \u03ba B nukle\u00e1ris bel\u00e9p\u00e9s\u00e9t is, ez\u00e1ltal elnyomja a gyullad\u00e1sos faktorok felszabadul\u00e1s\u00e1t \u00e9s g\u00e1tolja a szinovi\u00e1lis prolifer\u00e1ci\u00f3t. Yang \u00e9s munkat\u00e1rsai meg\u00e1llap\u00edtott\u00e1k, hogy a 300 p\u00e1lcika etanolos \u00e9s etil-acet\u00e1t kivonata g\u00e1tolja az \u00edz\u00fcleti duzzanatot CIA patk\u00e1nymodellekben, cs\u00f6kkenti a pro-gyullad\u00e1sos faktorokat, mint a TNF - \u03b1, IL-1 \u03b2 \u00e9s interleukin-6 (IL-6), \u00e9s n\u00f6veli az immunszuppressz\u00edv faktor interleukin-10 (IL-10) expresszi\u00f3j\u00e1t a sz\u00e9rumban. Mindezek a fentiek a h\u00e1romsz\u00e1z p\u00e1lca kiv\u00e1l\u00f3 gyullad\u00e1scs\u00f6kkent\u0151 \u00e9s reumaellenes hat\u00e1s\u00e1t bizony\u00edtj\u00e1k.<\/p>\n

Az autof\u00e1gia az a folyamat, amelynek sor\u00e1n az eukari\u00f3ta sejtek az autof\u00e1gi\u00e1val kapcsolatos g\u00e9nek szab\u00e1lyoz\u00e1s\u00e1val a lizosz\u00f3m\u00e1kat haszn\u00e1lj\u00e1k fel saj\u00e1t citoplazmatikus feh\u00e9rj\u00e9ik \u00e9s s\u00e9r\u00fclt organell\u00e1ik lebont\u00e1s\u00e1ra. Ez a folyamat k\u00e9pes lebontani a betolakod\u00f3 patog\u00e9n mikroorganizmusokat, s\u00e9r\u00fclt organell\u00e1kat \u00e9s abnorm\u00e1lisan felhalmoz\u00f3dott feh\u00e9rj\u00e9ket, \u00e9s fontos szerepet j\u00e1tszik olyan biol\u00f3giai folyamatokban, mint a sejtek min\u0151s\u00e9g\u00e9nek ellen\u0151rz\u00e9se, az anyagcsere, valamint a velesz\u00fcletett \u00e9s adapt\u00edv immunit\u00e1s. Sz\u00e1mos tanulm\u00e1ny meger\u0151s\u00edtette, hogy az autof\u00e1gia k\u00e9tir\u00e1ny\u00fa hat\u00e1st gyakorol a gyullad\u00e1sra: egyr\u00e9szt az autof\u00e1gia ellens\u00falyozhatja a gyullad\u00e1sos v\u00e1laszokat az\u00e1ltal, hogy elt\u00e1vol\u00edtja a gyullad\u00e1sos feh\u00e9rjeaggreg\u00e1tumokat \u00e9s leregul\u00e1lja a sz\u00f6vetk\u00e1rosod\u00e1st okoz\u00f3 pro-inflammatorikus citokineket; m\u00e1sr\u00e9szt az autof\u00e1gia aktiv\u00e1lja az inflammasz\u00f3m\u00e1kat, nagy mennyis\u00e9g\u0171 gyullad\u00e1sos faktort termelve, ez\u00e1ltal felgyors\u00edtva a gyullad\u00e1sos folyamatot. Az immunit\u00e1s \u00e9s a gyullad\u00e1s pozit\u00edv \u00e9s negat\u00edv aspektusainak kiegyens\u00falyoz\u00e1sa ut\u00e1n az autof\u00e1gia a fert\u0151z\u00e9s, az autoimmunit\u00e1s \u00e9s a gyullad\u00e1s v\u00e9delmez\u0151j\u00e9nek tekinthet\u0151. A mikrotubulushoz kapcsol\u00f3d\u00f3 feh\u00e9rje, a k\u00f6nny\u0171 l\u00e1nc 3-II (LC3-II) az autof\u00e1gia egyik jellegzetes feh\u00e9rj\u00e9je. Az autof\u00e1gia sor\u00e1n az LC3-I az Atg5-Atg12-Atg16 komplex seg\u00edts\u00e9g\u00e9vel egy foszfatidil-etanol molekul\u00e1hoz kapcsol\u00f3dik, \u00e9s \u00edgy alakul ki az LC3-II. A P62 az autof\u00e1gikus lebont\u00e1s szubsztr\u00e1tja, amely d\u00f6nt\u0151 szerepet j\u00e1tszik a lebontott szubsztr\u00e1tok felismer\u00e9s\u00e9ben \u00e9s bekapszul\u00e1z\u00e1s\u00e1ban. Ha a Beclin1-et eml\u0151ssejtekben t\u00falexpressz\u00e1lj\u00e1k, el\u0151seg\u00edti a sejtek autof\u00e1gi\u00e1j\u00e1t. Ez\u00e9rt az LC3, a Beclin1, a P62 \u00e9s az Atg5 az autof\u00e1gia markerfeh\u00e9rj\u00e9ik\u00e9nt szolg\u00e1lhatnak. Annak vizsg\u00e1lat\u00e1ra, hogy a TAAE \u00e1ltal kifejtett gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1s \u00f6sszef\u00fcgg-e az autof\u00e1gi\u00e1val, ebben a tanulm\u00e1nyban Western blot seg\u00edts\u00e9g\u00e9vel kimutattuk az autof\u00e1gi\u00e1val kapcsolatos P62, Beclin1, Atg5 \u00e9s LC3 feh\u00e9rj\u00e9k, valamint a gyullad\u00e1ssal kapcsolatos TNF - \u03b1, IL-6 \u00e9s ciklooxigen\u00e1z-2 (COX-2) feh\u00e9rj\u00e9k feh\u00e9rjeexpresszi\u00f3j\u00e1t. A k\u00eds\u00e9rleti eredm\u00e9nyek azt mutatt\u00e1k, hogy a TAAE beavatkoz\u00e1s ut\u00e1n a Beclin1, az Atg5 \u00e9s az LC3-II\/LC3- feh\u00e9rje expresszi\u00f3s szintje fokozatosan emelkedett, m\u00edg a szubsztr\u00e1t P62 feh\u00e9rje expresszi\u00f3s szintje fokozatosan cs\u00f6kkent, \u00e9s a gyullad\u00e1ssal kapcsolatos feh\u00e9rj\u00e9k expresszi\u00f3ja is cs\u00f6kkent. Az autofagosz\u00f3m\u00e1k jel\u00f6l\u00e9s\u00e9re szolg\u00e1l\u00f3 MDC-m\u00f3dszerrel \u00e9s az autofagosz\u00f3m\u00e1k megfigyel\u00e9s\u00e9re szolg\u00e1l\u00f3 transzmisszi\u00f3s elektronmikroszk\u00f3pi\u00e1val v\u00e9gzett k\u00eds\u00e9rleti eredm\u00e9nyek szint\u00e9n azt mutatt\u00e1k, hogy a TAAE el\u0151seg\u00edtette az autof\u00e1gi\u00e1t a RAW 264.7 sejtekben. Az autof\u00e1gia gyullad\u00e1sra gyakorolt hat\u00e1s\u00e1nak tov\u00e1bbi bizony\u00edt\u00e1sa \u00e9rdek\u00e9ben a makrof\u00e1g autof\u00e1gia kontroll\u00e1l\u00e1s\u00e1ra, az autof\u00e1gi\u00e1s kel\u00e1tk\u00e9pz\u0151d\u00e9s \u00e9s a feh\u00e9rj\u00e9k leboml\u00e1s\u00e1nak blokkol\u00e1s\u00e1ra a 3-MA autof\u00e1gia-inhibitort haszn\u00e1ltuk, amely egyben a PI3K jel\u00e1tviteli \u00fatvonal specifikus inhibitora is. Az eredm\u00e9nyek azt mutatt\u00e1k, hogy a 3-MA autof\u00e1gia-inhibitor gyeng\u00edtette a TAAE gyullad\u00e1sos citokinekre gyakorolt g\u00e1tl\u00f3 hat\u00e1s\u00e1t, m\u00edg a TAAE beavatkoz\u00e1s hat\u00e9konyan cs\u00f6kkentette a TNF - \u03b1 \u00e9s IL-6 citokinek szekr\u00e9ci\u00f3j\u00e1t a gyullad\u00e1sos modellben, ism\u00e9t bizony\u00edtva, hogy a TAAE gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1st fejt ki az autof\u00e1gia el\u0151seg\u00edt\u00e9s\u00e9vel a RAW 264.7 sejtekben.<\/p>\n

A PI3K\/AKT\/mTOR jel\u00e1tviteli \u00fatvonal fontos szerepet j\u00e1tszik az autof\u00e1gia szab\u00e1lyoz\u00e1s\u00e1ban, \u00e9s az autof\u00e1gia szintje fokoz\u00f3dik, ha a PI3K\/AKT\/mTOR \u00fatvonal g\u00e1tolt. Az MTOR a rapamycin eml\u0151s c\u00e9lpontja, \u00e9s fontos szab\u00e1lyoz\u00f3 szerepet j\u00e1tszik az autof\u00e1gia v\u00e1lasz\u00e1ban, az autof\u00e1gia kulcsfontoss\u00e1g\u00fa negat\u00edv szab\u00e1lyoz\u00f3 tengelyek\u00e9nt szolg\u00e1l. Sz\u00e1mos term\u00e9szetes term\u00e9kr\u0151l kimutatt\u00e1k, hogy a PI3K\/AKT\/mTOR \u00e1ltal k\u00f6zvet\u00edtett autof\u00e1gi\u00e1t c\u00e9lozva g\u00e1tolja a gyullad\u00e1st \u00e9s az autoimmun betegs\u00e9geket. Kor\u00e1bbi k\u00eds\u00e9rletek meger\u0151s\u00edtett\u00e9k, hogy a TAAE a PI3K\/AKT\/mTOR jel\u00e1tviteli \u00fatvonalon kereszt\u00fcl k\u00e9pes blokkolni az autof\u00e1gi\u00e1s \u00e1raml\u00e1st \u00e9s el\u0151seg\u00edteni az MH7A sejtek apopt\u00f3zis\u00e1t. A PI3K\/AKT\/mTOR jel\u00e1tviteli \u00fatvonalat Western blottinggal valid\u00e1ltuk, \u00e9s a k\u00eds\u00e9rleti adatok azt mutatt\u00e1k, hogy a TAAE jelent\u0151sen cs\u00f6kkentette a foszforil\u00e1lt PI3K, AKT \u00e9s mTOR expresszi\u00f3s szintj\u00e9t, ami azt jelzi, hogy a TAAE a PI3K\/AKT\/mTOR \u00fatvonal g\u00e1tl\u00e1s\u00e1val v\u00e1ltja ki az autof\u00e1gi\u00e1t. A PI3K agonista (740Y-P) egyidej\u0171 alkalmaz\u00e1sa tov\u00e1bb bizony\u00edtotta, hogy a TAAE a PI3K\/AKT\/mTOR jel\u00e1tviteli \u00fatvonal g\u00e1tl\u00e1s\u00e1val induk\u00e1lja az autof\u00e1gi\u00e1t. Ezenk\u00edv\u00fcl a PI3K\/AKT\/mTOR jel\u00e1tviteli \u00fatvonal k\u00f6zvetlen\u00fcl kapcsol\u00f3dik a gyullad\u00e1shoz \u00e9s az immunit\u00e1shoz. Ez a vizsg\u00e1lat meg\u00e1llap\u00edtotta, hogy a TAAE kezel\u00e9s cs\u00f6kkentette a pro-inflammatorikus citokinek szintj\u00e9t az LPS \u00e1ltal induk\u00e1lt RAW 264.7 sejtekben. Ez a vizsg\u00e1lat azt mutatja, hogy az LPS \u00e1ltal induk\u00e1lt RAW 264.7 sejtek gyullad\u00e1sos k\u00f6rnyezet\u00e9ben a TAAE g\u00e1tolja az autof\u00e1gi\u00e1val kapcsolatos PI3K\/AKT\/mTOR \u00fatvonalat, szab\u00e1lyozza az autof\u00e1gi\u00e1val kapcsolatos feh\u00e9rj\u00e9ket \u00e9s gyullad\u00e1sos faktorokat, el\u0151seg\u00edti az autofagosz\u00f3ma lizosz\u00f3ma f\u00fazi\u00f3j\u00e1t \u00e9s degrad\u00e1ci\u00f3j\u00e1t, befoly\u00e1solja a gyullad\u00e1sos sejtek homeoszt\u00e1zis\u00e1t, g\u00e1tolja a gyullad\u00e1sos v\u00e1laszokat, \u00e9s \u00edgy gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1st fejt ki. E tanulm\u00e1ny eredm\u00e9nyei azt sugallj\u00e1k, hogy a PI3K \/ AKT \/ MTOR hat\u00e9kony \u00fatvonal a TAAE sz\u00e1m\u00e1ra a gyullad\u00e1scs\u00f6kkent\u0151 hat\u00e1sok kifejt\u00e9s\u00e9re \u00e9s az autof\u00e1gikus aktivit\u00e1s n\u00f6vel\u00e9s\u00e9re, ami \u00faj \u00f6tleteket ny\u00fajthat a gyullad\u00e1ssal kapcsolatos autoimmun \u00e9s metabolikus betegs\u00e9gek klinikai kezel\u00e9s\u00e9hez, \u00e9s \u00e9rdemes tov\u00e1bbi m\u00e9lyrehat\u00f3 kutat\u00e1sra.<\/p>","protected":false},"excerpt":{"rendered":"

Three hundred rods based on PI3K\/AKT\/mTOR pathway promote lipopolysaccharide induced autophagy and inhibit inflammation in RAW264.7 cells Lipopolysaccharide (LPS) is an endotoxin released by Gram negative bacteria, which can stimulate immune inflammatory responses in bacterial toxicity caused by Gram negative bacterial infections in the human body. Macrophages often participate in inflammatory responses and phagocytosis, and […]<\/p>","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[20],"tags":[],"yoast_head":"\nThree hundred rods based on PI3K\/AKT\/mTOR pathway promote lipopolysaccharide induced autophagy and inhibit inflammation in RAW264.7 cells - China Chemical Manufacturer<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/longchangextracts.com\/hu\/three-hundred-rods\/\" \/>\n<meta property=\"og:locale\" content=\"hu_HU\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Three hundred rods based on PI3K\/AKT\/mTOR pathway promote lipopolysaccharide induced autophagy and inhibit inflammation in RAW264.7 cells - China Chemical Manufacturer\" \/>\n<meta property=\"og:description\" content=\"Three hundred rods based on PI3K\/AKT\/mTOR pathway promote lipopolysaccharide induced autophagy and inhibit inflammation in RAW264.7 cells Lipopolysaccharide (LPS) is an endotoxin released by Gram negative bacteria, which can stimulate immune inflammatory responses in bacterial toxicity caused by Gram negative bacterial infections in the human body. 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