突发新闻：2025年中东论文揭示伊维菌素如何杀死肺癌细胞！

2025年，Malak等人及其来自阿联酋、埃及和沙特阿拉伯的团队成员发表了一篇关于伊维菌素治疗肺癌的论文。

研究人员通过两次向免疫功能正常的 BALB/c 小鼠注射一种名为氨基甲酸乙酯（一种已知的致癌物，可模拟人类肺腺癌的特征）的化学物质，在小鼠体内诱发了肺癌。

他们将小鼠分成四组：

1. 正常健康对照组
2. 仅给予伊维菌素的健康小鼠
3. 癌症诱导小鼠（仅使用氨基甲酸乙酯）
4. 用伊维菌素治疗的致癌小鼠

伊维菌素研究的主要发现：

1. 肿瘤负荷降低，肺部健康状况改善

未经治疗的患癌小鼠肺部出现大量可见的肿瘤结节，肿瘤体积较大，肺部严重肿胀/发炎（通过“肺指数”测量——肺重量相对于体重，比正常情况高出约 56%）。

用伊维菌素治疗的癌症小鼠的肿瘤结节数量大大减少（降至未治疗癌症水平的约 66%），肿瘤体积也小得多（体积降至约 37 %) ，而且显微镜下可见的肿瘤团块数量也大幅减少（减少了 80%），肿瘤直径缩小了近 90%。

肺部炎症和肿胀急剧下降（肺部指数降至未治疗癌症水平的约 64%），表明伊维菌素减轻了损伤，并有助于在显微镜下保持正常的肺部结构。

2. 减缓癌症生长和扩散

快速细胞分裂标志物（Ki-67）在癌症小鼠体内激增，但经伊维菌素治疗后，其水平骤降至原水平的约37%。

3. 直接杀死癌细胞

肺癌损伤的血液标志物（CYFRA 21-1）在患癌小鼠体内急剧升高，但经伊维菌素治疗后显著下降。

伊维菌素通过增强促死亡蛋白（Bax 上调约 46%，活性 caspase-3 大幅上调约 442 %)来促进癌细胞凋亡（程序性细胞自杀），同时降低抗死亡蛋白（Bcl-2 下调约 78 %),从而使平衡向癌细胞死亡倾斜。

4. 阻断关键的癌症驱动通路

癌症激活了一条主要的生长通路（EGFR → PI3K → AKT → mTOR），从而促进肿瘤生长、存活、新血管形成（血管生成）和抵抗死亡。

在患癌小鼠中，EGFR 水平飙升（约高出 19 倍），下游蛋白质的活化形式也急剧增加。

伊维菌素强烈抑制了整个通路：EGFR 急剧下降，激活的 PI3K/AKT/mTOR 下降到癌症水平的 40-68%，VEGF（一种帮助肿瘤形成血管的蛋白质）显著减少。

5. 作者的总体结论

在这个小鼠模型中（与其他一些模型不同，该模型保持了免疫系统的完整性），伊维菌素发挥了强大的抗癌作用。

伊维菌素可缩小肿瘤、减轻炎症、减缓生长、触发癌细胞死亡，并关闭关键的生存/生长通路（EGFR/PI3K/AKT/mTOR/VEGF），同时还能促进细胞凋亡。

作者总结认为，伊维菌素有望成为治疗非小细胞肺癌的药物，并呼吁开展更多研究，包括人体临床试验。

@FLSurgeonGen

BREAKING NEWS: 2025 Paper from Middle East identifies how Ivermectin kills Lung Cancer cells!

In 2025, Malak et al. with a team from UAE, Egypt and Saudi Arabia, published a paper on Ivermectin in Lung Cancer

The researchers created lung cancer in immune-normal BALB/c mice by injecting them twice with a chemical called urethane (a known carcinogen that mimics features of human lung adenocarcinoma).

They divided the mice into four groups:

1. Normal healthy controls
2. Healthy mice given Ivermectin only
3. Cancer-induced mice (urethane only)
4. Cancer-induced mice treated with Ivermectin

KEY FINDINGS from IVERMECTIN:

1. Reduced Tumor Burden and Better Lung Health

Untreated cancer mice developed lots of visible tumor nodules on the lungs, with large tumor sizes and severe lung swelling/inflammation (measured by “lung index” — lung weight relative to body weight, up ~56% higher than normal).

Ivermectin-treated cancer mice had far fewer tumor nodules (down to ~66% of untreated cancer levels), much smaller tumors (volume down to ~37%), and dramatically less microscopic tumor masses (80% fewer) with tumor diameters shrunk by nearly 90%.

Lung inflammation and swelling dropped sharply (lung index reduced to ~64% of untreated cancer levels), showing ivermectin calmed the damage and helped preserve normal lung structure under the microscope.

2. Slowed Cancer Growth and Spread

A marker of fast cell division (Ki-67) exploded in cancer mice but plummeted to ~37% of that level with Ivermectin

3. Killed Cancer Cells Directly

A blood marker for lung cancer damage (CYFRA 21-1) rose sharply in cancer mice but fell significantly with Ivermectin treatment.

Ivermectin promoted apoptosis (programmed cell suicide) in cancer cells by boosting pro-death proteins (Bax up ~46%, active caspase-3 up massively ~442%) while lowering the anti-death protein (Bcl-2 down to ~78%), flipping the balance toward cancer cell death.

4. Blocked Key Cancer-Driving Pathways

Cancer activates a major growth pathway (EGFR → PI3K → AKT → mTOR), which fuels tumor growth, survival, new blood vessel formation (angiogenesis), and resistance to death.

In Cancer mice, EGFR levels skyrocketed (~19x higher), and the activated forms of the downstream proteins increased dramatically.

Ivermectin strongly suppressed this entire pathway: EGFR dropped sharply, activated PI3K/AKT/mTOR fell to 40–68% of cancer levels, and VEGF (a protein that helps tumors build blood vessels) decreased significantly.

5. Overall Conclusions from the Authors

In this mouse model (which keeps the immune system intact, unlike some other models), Ivermectin acted as a powerful anti-cancer agent.

Ivermectin shrank tumors, reduced inflammation, slowed growth, triggered cancer cell death, and shut down a critical survival/growth pathway (EGFR/PI3K/AKT/mTOR/VEGF), while also promoting apoptosis.

The authors conclude Ivermectin shows promise as a repurposed drug for NSCLC Lung Cancer and call for more studies, including human clinical trials.

@FLSurgeonGen @MakisMedicine