Objective The present study aimed to evaluate the efficacy and safety of azilsartan (Azil) as “add-on” treatment with methotrexate (MTX) in patients with active rheumatoid arthritis (RA). MethodsThis single center, randomized, placebo-controlled, double-blind, pilot study included 64 patients with active RA. Patients received either placebo or Azil in addition to their currently used MTX doses for 90 days. The primary outcomes were DAS-28, SDAI, HAQ-DI, CDAI, EGA, and swollen and tender joints count. The secondary outcomes were the changes in the pain visual analogue scale (VAS-100), serum levels of TNF-α, IL-1β, IL-6, and anti-CCP, the lipid profile, and the markers of kidney and liver functions in the two groups at baseline and after 90 days. ResultsAfter 90 days, most clinical scores were significantly better in the Azil-treated group than in the placebo group. All inflammatory biomarkers were significantly improved after treatment with MTX + Azil compared to baseline and placebo group. No safety concerns were reported during the study period. Conclusions Azilsartan improved the effects of methotrexate on the clinical scores and certain inflammatory biomarkers of patients with active RA. Trial Registration The protocol was registered under the number 507/SA/1024 at the local clinical studies database, College of Medicine, Sulaimani University.

Background and aimMuch evidence has emerged documenting the involvement of the renin-angiotensin system (RAS) in inflammatory processes. The objective of this study was to evaluate the effects of blocking RAS with azilsartan (Azil) on the clinical efficacy of etanercept (Etan) in patients with active rheumatoid arthritis (RA).Patients and methodsForty-two patients diagnosed with active RA and poorly responding to methotrexate were enrolled in this pilot clinical study. They were randomly allocated into two groups, and treated with either Etan (50 mg/week) and placebo or the same dose of Etan with Azil (20 mg/day) for 90 days. The clinical outcome was evaluated using the Disease Activity Score-28 joint (DAS-28), simplified disease activity index (SDAI), clinical disease activity index (CDAI) and the health assessment questionnaire disease index (HAQ-DI). Blood samples were obtained for the assessment of C-reactive protein and erythrocyte sedimentation rate at baseline and after 90 days.ResultsThe markers of pain and disease activity, C-reactive protein and erythrocyte sedimentation rate were significantly improved when Azil was used, as an adjuvant with Etan, compared with the use of Etan and placebo.ConclusionBlocking RAS with azilsartan may improve the effects of etanercept on the clinical markers of pain and disease severity of patients with active RA not responding to methotrexate.

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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.

Breast cancer has the highest prevalence of all cancers in females, with roughly 2.26 million new cases diagnosed and an estimated 0.68 million deaths/year. Hormone receptor-positive (HR+) or human epidermal growth factor receptor-negative (HER2-) illness affects the vast majority of patients with metastatic breast cancer (MBC). Endocrine therapy (ET) with aromatase inhibitors (AIs) is the preferred first-line choice for this subpopulation. However, because most patients developed tolerance to these medications, demand for alternate endocrine regimens has surged. Inhibition of cyclin-dependent kinase 4 and 6 (CDK4/6) is proving to be a success in resistant patients as well as a first-line treatment. This review article highlights the current indications for CDK4/6 inhibitors in breast cancer that have been approved by the FDA. The literature search was confined to the years 2015 to 2020, and 27 articles and 6 studies were chosen for further research from a large number of publications. In hormone receptor-positive, HR RC+, HER2- advanced or metastatic breast cancer (ABC/MBC) patients, the use of currently available CDK4/6 inhibitors, either alone (abemaciclib) or in combination with endocrine therapy (Palbociclib and Ribociclib), showed a beneficial effect when compared to endocrine therapy alone. The use of CDK4/6 inhibitors resulted in longer progression-free survival (PFS), greater clinical benefit rates (CBR), and an overall response rate (ORR), as well as an overall survival (OS) advantage in patients previously treated with endocrine treatment (ET).

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.

Diabetes mellitus (DM) with uncontrolled blood sugar causes a variety of problems, including coronary artery disease, stroke, heart failure, hypertension, nephropathy, neuropathy, and retinopathy. These consequences harm the diabetic patients' lives. Many studies have shown that diabetic patients have a higher rate of heart failure and a worse prognosis than non-diabetic people. Sodium and glucose co-transporter receptor-2 (SGLT2) inhibitors are a relatively new class of anti-diabetic drugs. They not only regulate blood sugar but also have positive cardiovascular effects via a variety of mechanisms. This review intends to show that SGLT2 inhibitors, in addition to good glycemic control, possess a cardioprotective role. We conducted a literature review and identified 20 adequately powered clinical trials and animal studies in type 2 DM that investigated the cardiovascular (CV) effects of SGLT2 inhibitors (particularly heart failure and hypertension). These studies looked at the cardiovascular effects of three SGLT2 inhibitors: Empagliflozin, Canagliflozin, and Dapagliflozin. In diabetic patients, these three inhibitors of SGLT2 significantly lowered the risk of heart failure and hypertension, making them valuable therapy for lowering CV risks in high cardiovascular-risk individuals with T2DM. Finally, the use of SGLT2 inhibitors in patients without diabetes mellitus showed positive metabolic outcomes in weight and blood pressure control.

Background The local renin-angiotensin system has been discovered in the eyes; thus, this study evaluates the Azilsartan effect in the retina and optic nerve toxicity induced by Cisplatin in vivo. Methodology Forty-eight male rats were randomly assigned into six groups of 8 animals. Group 1 was healthy control that received 0.5 mL/day of 0.5% carboxymethyl cellulose (CMC) orally (PO). Group 2 received a single dose of the 7.0 mg/kg CIS intraperitoneally with 0.5 mL/day of 0.5% CMC-PO. Groups 3 and 4 received 3.5 and 7.0 mg/kg/day of AZIL-PO, respectively. Groups 5 and 6 received 3.5 and 7.0 mg/kg/day of AZIL-PO, respectively together with a single dose of 7.0 mg/kg of CIS-IP. The ocular tissue and serum estimated the TNF-α, NF-kβ, and Casp-3. A complete blood count was also measured, and the eye was sent for histological examination. Results The administration of the 3.5 mg/kg AZIL significantly ( p < 0.05) reduced the ocular tissue and serum TNF-α, NF-kB, and Casp-3 levels, when given to CIS treated group, while the 7.0 mg/kg AZIL does not. Additionally, azilsartan shows no negative impact on the CBC in rats. Finally, the eye histological examination showed a significant ( p < 0.05) drop in the signs of inflammation and cellular degeneration, particularly after administration of the 3.5 mg/kg AZIL to the CIS-treated group. Conclusion A low dose of AZIL exerts an anti-inflammation and an anti-apoptotic effect through significant suppression of the pro-inflammatory mediators and an apoptotic biomarker by blocking the local angiotensin II type