相关实验视频

Updated: Jun 22, 2025

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

Published on: May 3, 2024

大麻醇通过抑制PI3K/Akt/NF-κB介导的烧灭症来缓解口腔粘膜炎

Jialin Yang¹, Na Lin¹, Shuang Li²

¹Mudanjiang Medical University School of Stomatology, Mudanjiang, China.

Balkan medical journal

|July 5, 2024

概括

大麻 (CBD) 通过抑制PI3K/Akt/NF-κB通路和热,减少炎症和改善细胞健康,有效治疗口腔粘膜炎 (OM).

科学领域:

药理学药理学是指药理学的学科.
分子生物学分子生物学
在瘤学瘤学.

背景情况:

Cannabidiol (CBD) 是来自Cannabis sativa的衍生物,具有已知的抗癌,抗炎和止痛特性.
在缓解口腔粘膜炎 (OM) 中,CBD的精确治疗机制仍然不完全理解.

研究的目的:

在小鼠模型中研究CBD对口腔粘膜炎 (OM) 的治疗作用.
阐明CBD对人类口腔角质细胞 (HOK) 细胞作用的分子机制.

主要方法:

使用多个数据库 (TCM系统药理学,GeneCard,DisGeNET,GEO) 来识别目标基因和构建网络.
在体内通过炎症标志物,组织学分析和基因/蛋白质表达来评估OM的严重程度.
在实验室中评估了HOK细胞的增殖,迁移,亡和烧亡,并进行分子通路分析 (Western blot,qRT-PCR).

主要成果:

确定了49个重叠的基因,NF-κB1,PIK3R1,NF-κBIA和AKT1作为关键的枢纽基因,涉及PI3K/Akt/NF-κB和IL-17通路.
在体内,CBD显著减少了病变区域,减轻了组织损伤,并降低了NLRP3,P65,AKT和PI3K的调节.
在体外,CBD促进了HOK细胞的增殖和迁移,同时通过PI3K/Akt/NF-κB通路的抑制降低了亡和热亡.

结论:

通过抑制PI3K/Akt/NF-κB信号通路和热,CBD显示出一种用于OM管理的新机制.
这些行动共同减轻了OM症状,突出了CBD的治疗潜力.

更多相关视频

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

相关概念视频

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

Chemotherapy-Induced Nausea and Vomiting: Cannabinoids

Tetrahydrocannabinol (THC) is a phytocannabinoid that primarily interacts with the CB1 receptor, a type of G protein-coupled receptor (GPCR) predominantly in and around the chemoreceptor trigger zone (CTZ) and emetic center. THC also blocks the serotonin receptor activity in the dorsal vagal complex (DVC) by inhibiting serotonin release. THC exerts its anti-emetic effects through these interactions, which are beneficial for patients undergoing chemotherapy.
Two synthetic agonists of THC,...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates...

Drugs that Stabilize Microtubules

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...