Alam Mohammad Firoz, Ajeibi Ahmed O, Safhi Majed H, Alabdly Ahmad J A, Alshahrani Saeed, Rashid Hina, Qadri Marwa, Jali Abdulmajeed M, Alqahtani Saud, Nomier Yousra, Moni Sivakumar S, Khalid Mohammad, Anwer Tarique
Department of Pharmacology and Toxicology, College of Pharmacy, Jazan University, Jazan 45142, Saudi Arabia.
Department of Pharmacology, College of Pharmacy, King Khalid University, Abha 61421, Saudi Arabia.
J Clin Med. 2023 Jan 24;12(3):911. doi: 10.3390/jcm12030911.
Cyclophosphamide (CPM) is a classical alkylating agent used in different cancer chemotherapy regimens and is restricted due to severe adverse effects, including hepatotoxicity. Natural or plant-derived antioxidants such as capsaicin were utilized in this study to examine the hepatoprotective benefits against cyclophosphamide-induced hepatotoxicity. The rats were divided into five groups: a normal control group, a toxic group (CPM), an intraperitoneal injection of a single dose of 200 mg/kg b.w. on the fourth day, a pretreated group with two doses of CPS (10 mg and 20 mg/kg b.w.) orally for six consecutive days, and an intraperitoneal administration of 200 mg/kg b.w. on the fourth day of treatment. The fifth group was administered with the highest dose of CPS (20 mg/kg b.w.) orally for six consecutive days. After 24 h of administration of CPS, the rats were anesthetized, blood was collected, and the serum enzyme toxicity was evaluated. After the blood sampling and euthanasia of all the animals, the liver was isolated for further toxicity and histopathological examination. The results revealed that serum liver markers (AST, ALT, ALP, BLI) significantly increased after CPM administration, but were subsequently restored after CPS treatment with both doses. In addition, lipid peroxidation (MDA), inflammatory cytokines (IL-1β, TNF-α), and apoptotic markers (Caspase-3) increased, and antioxidant enzymes (GSH, CAT, SOD) were significantly decreased after CPM administration, and it was re-established by CPS treatment. However, CPS effectively protected against the CPM-induced histopathological architects of liver tissues. In conclusion, CPS attenuates CPM-induced hepatotoxicity via modulating oxidative stress, apoptotic signals, and cytokine pathway. Therefore, CPS could play a significant role as a supplement during the chemotherapy of patients.
环磷酰胺(CPM)是一种用于不同癌症化疗方案的经典烷化剂,但因其包括肝毒性在内的严重不良反应而受到限制。本研究使用了天然或植物来源的抗氧化剂如辣椒素,以检验其对环磷酰胺诱导的肝毒性的保肝作用。大鼠被分为五组:正常对照组、毒性组(CPM),于第4天腹腔注射单剂量200mg/kg体重;预处理组,连续6天口服两剂CPS(10mg和20mg/kg体重),并于治疗第4天腹腔注射200mg/kg体重。第五组连续6天口服最高剂量的CPS(20mg/kg体重)。在给予CPS 24小时后,将大鼠麻醉、采血并评估血清酶毒性。在所有动物采血和安乐死后,分离肝脏进行进一步的毒性和组织病理学检查。结果显示,给予CPM后血清肝标志物(AST、ALT、ALP、BLI)显著升高,但在用两种剂量的CPS治疗后随后恢复。此外,给予CPM后脂质过氧化(MDA)、炎性细胞因子(IL-1β、TNF-α)和凋亡标志物(Caspase-3)增加,抗氧化酶(GSH、CAT、SOD)显著降低,而CPS治疗使其恢复。然而,CPS有效保护了肝脏组织免受CPM诱导的组织病理学结构破坏。总之,CPS通过调节氧化应激、凋亡信号和细胞因子途径减轻CPM诱导的肝毒性。因此,CPS在患者化疗期间可作为一种重要的补充剂发挥作用。