Unfortunately, anticancer medications are extremely harmful to normal cells. Doxorubicin (DOX) is a highly cardiotoxic medication that can result in cardiomyopathy. The most significant mechanism for DOX-induced cardiotoxicity is oxidative stress, while other pathways have also been put forth. This review aims to highlight the mechanisms of DOX-induced cardiotoxicity and the most updated managements. Trustworthy sites such as Google Scholar, PubMed, and Research Gate were used to find the most updated articles. Many titles have been used for searching, such as "doxorubicin and cardiotoxicity," "cardioprotection," and "cardio-protective effects of phytochemicals." Preprints, review articles, and research with meta-analyses were disregarded. Three pathways, including oxidative stress, mitochondrial damage, and calcium excess, were responsible for DOX-induced cardiotoxicity. Cardiotoxicity may be partially caused by cell death, activation of the ubiquitin-ligase-proteasome system, and changes in its gene expression brought on by DOX. In the instance of DOX cardiotoxicity, medications and nutraceuticals with antioxidants and iron chelating properties have been found to have cardio-protective benefits. In conclusion, doxorubicin-treated cancer patients have been linked to cardiotoxicity, making cardioprotection extremely important in these patients. All of the mechanisms included in this review's discussion might provide light on fresh approaches to the treatment and/or prevention of DOX-induced cardiotoxicity.

The effects of thymoquinone (TQ) in a carcinogen-based models of urinary bladder cancer were evaluated, using 45 male rats in five groups. In negative control ( n = 10), only tap water was given. In positive control ( n = 10), the rats received 0.05% N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) in drinking water for 9 weeks. In preventive groups with 25 mg/kg ( n = 10) and 50 mg/kg ( n = 10), oral TQ was concurrently given with 0.05% BBN for 9 weeks and continued for one more week after cessation of BBN. Preventive-treatment group ( n = 5) received 50 mg/kg TQ orally for 20 weeks. Five rats from each group were sequentially sacrificed in two phases: the induction phase at 12th week (except the last group) and the rest in postinduction phase at 20th week. The bladders were examined macroscopically for lesion formation, and the masses were submitted for histopathological evaluation. Markers for total oxidant status (TOS), inflammation (nuclear factor kappa B (NF- κ B)), and angiogenesis (vascular endothelial growth factor (VEGF)) were also assessed. There was a reduced number of bladder lesions in the TQ groups versus the carcinogen group at both phases. Histopathological findings demonstrated a significant improvement in the abnormal morphological changes in the urothelium of the TQ-treated groups. Thymoquinone exerted a significant antioxidant and anti-inflammatory effect by a decrease in serum level of TOS and NF- κ B at week 12 which was maintained low in phase two at week 20. The serum level of VEGF was also alleviated in the induction phase at week 12 and maintained low in postinduction period. In TQ preventive-treatment approach, a nonsignificant elevation of serum level of TOS and NF- κ B and slight reduction in VEGF were observed at the end of the experiment. These data suggest that TQ may be effective in preventing bladder carcinogenesis, and the suggested mechanisms might be related to antioxidant, prooxidant, and anti-inflammatory properties of TQ.

Background: Pollution and genetic factors have increased the likelihood of cancer in the developing world. Cancer is now the leading cause of death in young patients. Scientists are focusing on developing new treatments with a lower risk profile than traditional cytotoxic drugs. Nigella sativa (black seed) has been used for centuries by ancient cultures to treat a variety of ailments. Thymoquinone, the main active compound found in Nigella sativa, is a useful therapeutic agent for various morbidities, including cancer. Aim: The review aims to highlight thymoquinone's potential cytotoxic and chemoprotective effects. Methods: The most recent articles were found using reputable websites such as Google Scholar, PubMed, and Research Gate. Many titles, such as thymoquinone, breast cancer, leukemia, colon cancer, osteosarcoma, ovary cancer, and so on, have been used in searches. Then the information from in vitro studies and animal experiments was collected; the preprint, article review, and meta-analysis study were all excluded. Results: Thymoquinone reduced cell viability and induced programmed cell death in breast cancer, colon cancer, leukemia, osteosarcoma, ovary cancer, and colon cancer. TQ causes cytotoxicity through a variety of mechanisms, including the induction of reactive oxygen species and the inhibition of NF-kB activity in some cancers. Conclusion: Thymoquinone is a promising future cytotoxic agent with fewer side effects than traditional cytotoxic agents.

The renin-angiotensin system (RAS) was thought to be in charge of managing blood pressure and electrolytes. It has been established that angiotensin II is also responsible for controlling inflammation in addition to blood pressure and potassium levels. Angiotensin converting enzyme 2 (ACE2), angiotensins (1–7), angiotensins (1–9), and other additional RAS components have been identified, and have anti-angiotensin II effects. Both angiotensin receptor blockers (ARBs) and angiotensin converting enzyme inhibitors (ACEIs) are utilized as anti-hypertensive medications and protecting the heart and kidneys, and counteract the part played by Ang II in the initiation of inflammation. This review provides crucial details that help explain how ACEI and ARBs reduce inflammation. Using reliable websites like Google Scholar, PubMed, and ResearchGate, the most recent publications were reviewed. Search terms have included "RAS role of Ang II in inflammation," "influence of ACEI," and "effect of ARBs on PPAR-gamma." The data were gathered from controlled clinical trials, in vitro studies, and animal-based studies; preprints, article reviews, and meta-analysis studies were excluded. Both ACEIs and ARBs reduce inflammation via a variety of mechanisms, which explains their cardioprotective and nephroprotective effects. They reduce inflammation by modulating an inflammatory pathway through either similar or dissimilar mechanisms.