大量的证据表明，压力调节激素，包括肾上腺素，在多种癌症的发展中发挥着重要作用，包括T细胞淋巴瘤。此外，廉价的β-肾上腺素能受体拮抗剂普萘洛尔也被报道具有抗肿瘤和化疗增敏作用，可用于乳腺癌、结肠癌、卵巢癌和胰腺癌等疾病的治疗。然而，普萘洛尔在包括T细胞淋巴瘤在内的血液系统恶性肿瘤中的体内抗肿瘤和化疗增敏活性尚未得到研究。因此，本研究旨在评估普萘洛尔在一种T细胞淋巴瘤小鼠模型中的抗肿瘤和化疗增敏作用。在本研究中，采用T细胞淋巴瘤携带小鼠，分别用纯溶液（PBS）和含有普萘洛尔的纯溶液进行治疗，然后进行铂类药物顺铂的给药治疗。评估肿瘤的进展，并对肿瘤细胞凋亡、葡萄糖代谢、pH调节和抗肿瘤免疫反应进行分析。通过Wright-Giemsa、annexin-V和DAPI染色对细胞和核形态进行评估百胜彩票。采用ELISA检测血清中肾上腺素水平。通过色度学方法测量肿瘤腹水中的葡萄糖、乳酸和NO水平。采用RT-PCR和Western blot评估各种重要调节因子在基因和蛋白水平的表达量。我们的结果表明，普萘洛尔通过改变凋亡、糖酵解、肿瘤微环境的酸化和免疫抑制，对DL携带小鼠具有抗肿瘤和化疗增敏的能力。版权所有 © 2023 Elsevier B.V. 保留所有权利。

Accumulating evidence has shown a vital role of stress-regulatory hormones, including epinephrine, in the progression of numerous cancers, including T cell lymphoma. Further, the antitumor and chemosensitizing potential of propranolol, an inexpensive β-adrenergic receptor antagonist has also been reported against breast, colon, ovarian, and pancreatic cancers. However, in vivo antitumor and chemopotentiating activity of propranolol have not yet been examined against malignancies of hematological origin, including T cell lymphoma. Therefore, the present study is designed to evaluate the antitumor and chemopotentiating action of propranolol in a T cell lymphoma murine model. In this study, T cell lymphoma-bearing mice were treated with vehicle alone (PBS) or containing propranolol followed by administration of with or without cisplatin. The progression of the tumor was assessed along with analysis of tumor cell apoptosis, glucose metabolism, pH regulation, and antitumor immune response. The apoptosis was estimated by cellular and nuclear morphology analysis through Wright-Giemsa, annexin-V, and DAPI staining. ELISA was used to detect the epinephrine level in serum. The glucose, lactate, and NO levels were measured in the tumor ascitic fluid by calorimetric methods. RT-PCR and Western blot were used to assess the levels of various crucial regulators at gene and protein levels, respectively. Our results showed that propranolol exerts antitumor as well as chemopotentiating ability in DL-bearing mice by altering apoptosis, glycolysis, acidification of TME, and immunosuppression.Copyright © 2023 Elsevier B.V. All rights reserved.