Alherz Fatemah A, Elekhnawy Engy, Selim Hend Mostafa, El-Masry Thanaa A, El-Kadem Aya H, Hussein Ismail A, Negm Walaa A
Department of Pharmaceutical Sciences, College of Pharmacy, Princess Nourah Bint Abdulrahman University, P.O. Box 84428, Riyadh 11671, Saudi Arabia.
Pharmaceutical Microbiology Department, Faculty of Pharmacy, Tanta University, Tanta 31527, Egypt.
Pharmaceuticals (Basel). 2023 Aug 18;16(8):1180. doi: 10.3390/ph16081180.
Acute kidney injury (AKI) is one of the major side effects of cisplatin, a remarkable anticancer agent. Therefore, there is a growing need to find an agent that could mitigate cisplatin-induced nephrotoxicity. Betulinic acid (BA) is a natural compound isolated from Forssk for the first time, with miraculous biological activities and no reports of its effect on the nephrotoxicity induced by cisplatin. Mice received BA orally with doses of 30 and 50 mg/kg before the intraperitoneal injection of cisplatin. Betulinic acid was found to decrease serum levels of creatinine and tissue levels of NGAL and kidney injury molecule (KIM-1) and improve the histological changes in the kidney. In addition, BA decreased the oxidative stress marker malondialdehyde (MDA), increased superoxide dismutase (SOD) antioxidative activity and suppressed the intensity of IL-1B and NFкB immuno-staining. Interestingly, betulinic acid enhanced autophagy by increasing beclin 1, ATG5, and LC3II and decreasing p62 expressions. Thus, our findings suggest betulinic acid as a potential agent that may protect from acute kidney injury by targeting inflammation, oxidative stress, and autophagy processes. Novel drugs are needed to combat the spreading of multidrug resistance between pathogenic bacteria, especially uropathogenic isolates. So, we elucidated the antibacterial properties of BA on , , , and . Betulinic acid had minimum inhibitory concentration values (128 to 512 µg/mL). In addition, it adversely affected the membrane integrity of the tested isolates. Accordingly, betulinic acid should be clinically investigated in the future for urinary tract diseases.
急性肾损伤（AKI）是顺铂（一种显著的抗癌药物）的主要副作用之一。因此，越来越需要找到一种能够减轻顺铂诱导的肾毒性的药物。桦木酸（BA）是首次从Forssk中分离出的一种天然化合物，具有神奇的生物活性，且尚无关于其对顺铂诱导的肾毒性影响的报道。在腹腔注射顺铂之前，给小鼠口服30和50 mg/kg剂量的BA。发现桦木酸可降低血清肌酐水平、NGAL和肾损伤分子（KIM-1）的组织水平，并改善肾脏的组织学变化。此外，BA降低了氧化应激标志物丙二醛（MDA），增加了超氧化物歧化酶（SOD）的抗氧化活性，并抑制了IL-1B和NFкB免疫染色的强度。有趣的是，桦木酸通过增加beclin 1、ATG5和LC3II并降低p62表达来增强自噬。因此，我们的研究结果表明桦木酸作为一种潜在的药物，可能通过针对炎症、氧化应激和自噬过程来预防急性肾损伤。需要新型药物来对抗病原菌之间多重耐药性的传播，尤其是尿路致病性分离株。因此，我们阐明了BA对[此处原文缺失具体细菌名称]、[此处原文缺失具体细菌名称]、[此处原文缺失具体细菌名称]和[此处原文缺失具体细菌名称]的抗菌特性。桦木酸的最低抑菌浓度值为128至512 µg/mL。此外，它对受试分离株的膜完整性有不利影响。因此，桦木酸未来应针对尿路疾病进行临床研究。
