Objectives: Acute peritonitis remains a critical condition with high mortality rates, further complicated by the rising antibiotic resistance. This study aimed to investigate the therapeutic potential of Chlorella vulgaris (CHL), both alone and in combination with standard antibiotic therapy (SFT), in a rat model of cecal ligation and puncture (CLP)-induced peritonitis. Methods: Seventy (70) male Wistar albino rats were divided into seven groups (n = 10): Control, Peritonitis Control, Low-dose CHL (CHL I) (150 mg/kg), High-dose CHL (CHL II) (300 mg/kg), the standard first-line therapy group (SFT) (Ceftriaxone + Metronidazole), SFT + CHL I, and SFT + CHL II. Following CLP-induced peritonitis, treatments were administered for 7 days. Peritoneal tissues were evaluated histopathologically and immunohistochemically for TNF-α, IL-1β, IL-10, and iNOS expression. Total Antioxidant Status (TAS) and Total Oxidant Stress (TOS) were measured to assess the oxidative stress. Results: Histopathological analysis showed that CLP-induced severe inflammatory damage was significantly reduced in all treatment groups, with the most prominent recovery observed in the SFT + CHL II group. CHL treatment led to a significant decrease in pro-inflammatory markers (TNF-α, IL-1β, iNOS) compared to the peritonitis control group (PC) (p < 0.05). Furthermore, CHL administration significantly improved the oxidative balance by increasing TAS and reducing TOS levels. Conclusions: Chlorella vulgaris exhibits significant anti-inflammatory, antioxidant, and immunomodulatory properties in experimental peritonitis. When used as an adjunct to standard antibiotic therapy, high-dose CHL provides synergistic effects that contribute to limiting tissue damage and controlling systemic inflammation. These findings suggest that CHL may be a promising supportive agent in the clinical management of acute peritonitis.

This study aims to assess the pharmacodynamics of aucubin, the active ingredient in plantain (Plantago), on in vitro rat bladder and trachea tissues, and explore its cell protective effects on primary lung and kidney cell lines. The study was carried out via repeated applications of acetylcholine, atropine, verapamil and oxybutynin, alongside Ca++ in a calcium-free environment, on urinary bladder tissue, and repeated applications of acetylcholine, atropine, carbachol and mecamylamine on trachea tissue. At the same time, cell viability and catalase and superoxide dismutase activity was measured on primary cell lines. The results indicate that aucubin has a relaxant effect on urinary bladder and trachea tissues. It is conceived that aucubin acts as a cholinergic antagonist through different subreceptors (muscarinic-3 receptors). The results also indicate that aucubin has a dose-dependent effect on primary lung and kidney cell lines, with increased cell viability, reduced cytotoxicity and antioxidant effects. In conclusion, it is suggested that plantain, which is used in folk medicine, and its active ingredient aucubin might have beneficial effects on bronchoconstriction and other respiratory conditions, as well as on pulmonary and renal diseases, urinary incontinence, etc.

Deneysel renal iskemi/reperfüzyon (IR) modeli, böbreğin iskemik koşullardan ve ardından gelişen reperfüzyon hasarından etkilenme düzeyini taklit etmek için kullanılan önemli bir yöntemdir. Bu model, böbrek transplantasyonunda donör organ hasarı, renal arter/vena üzerindeki basılar veya böbreklere olan kan akışını engelleyen çeşitli klinik durumları deney hayvanlarında simüle etmeye olanak tanır. Ayrıca, böbrek iskemisinin uzak dokularda yol açtığı hasarı incelemek için de gereklidir. İskemi, bir dokuya olan arteriyel veya venöz dolaşımın (ya da her ikisinin) mekanik olarak kısıtlanmasıdır. Hasarın şiddeti, iskeminin süresi, kısıtlanmanın derecesi ve yerine bağlı olarak değişir. Örneğin, arteriyal dolaşımın kısıtlanması dokunun beslenememesine yol açarken venöz dolaşım kısıtlaması, dokuda toksik metabolitlerin birikimine sebep olarak hasara neden olabilir. Kan akışının yeniden sağlanması olan reperfüzyon, hayat kurtarıcı olmasına rağmen, maalesef tek başına faydalı değildir. Reperfüzyon aşamasında da ciddi doku hasarı meydana gelebilir; hatta uzak organ hasarının büyük bir kısmı bu reperfüzyon hasarına atfedilir. Bunun nedeni, iskemi sırasında biriken toksik metabolitlerin, yeniden dolaşıma katılım (reperfüzyon) fazında sistemik dolaşıma karışarak sistemik hasarı tetiklemesidir. The experimental renal ischemia/reperfusion (IR) model is a pivotal tool used to simulate the extent of kidney damage following ischemic conditions or subsequent reperfusion injury. While frequently employed to assess direct renal damage, it is also essential for investigating remote organ injury stemming from renal ischemia. This model allows for the simulation of diverse clinical scenarios in animal subjects, including the damage sustained by a donor kidney during transplantation under ischemic storage, unilateral or bilateral kidney ischemia resulting from mechanical pressure on the renal artery or tumor pathologies, and the ischemic conditions caused by swelling due to urinary tract stenoses. Ischemia is generally defined as the mechanical restriction of arterial, venous, or combined blood flow to a specific tissue. The duration and degree of this restriction determine the severity of ischemic damage, ranging from tissue injury to complete necrosis. The location of the restriction is also crucial; arterial occlusion leads to tissue starvation, whereas venous occlusion can cause damage through the accumulation of toxic metabolites. Paradoxically, while reperfusion (the restoration of blood flow) is life-saving, it is not entirely beneficial. Reperfusion itself can induce significant tissue damage. This reperfusion injury is often held responsible for a large portion of remote organ damage. During the ischemic phase, local damage occurs, but systemic effects are limited due to restricted perfusion. However, upon reperfusion, the toxic metabolites accumulated in the ischemic tissue are released into the systemic circulation, thereby initiating a cascade of systemic injury.

Farmakokinetik temelde vücudun ilaca ne yaptığını inceleyen bilim dalıdır. Temel olarak emilim (absorbsiyon), dağılım (distribüsyon), metabolizma (biyotransformasyon), atılım (eliminasyon) olmak üzere dört ana süreçten oluşur ve ADME kısaltmasıyla ifade edilir. Emilim ilacın uygulandığı yerden (oral, parenteral, deri gibi) kan dolaşımına geçişidir. Emilimin hızı ise birçok faktöre göre değişiklik göstermektedir. Dağılım ilacın kan dolaşımı aracılığıyla dokulara yayılmasıdır. Bu süreçte kan proteinlerine bağlanma, dokuların ilaca olan ilgisi ve kan-beyin bariyeri gibi faktörler önemli bir yere sahiptir. Dağılım hacmi (Vd), ilacın vücutta ne kadar geniş alana yayıldığını gösterir. Metabolizma (biyotransformasyon) ilacın genellikle karaciğerde kimyasal olarak değiştirilmesidir. Bu süreçte enzimler (özellikle sitokrom P450 sistemi) önemli rol oynar. Bazı ilaçlar daha etkili hale gelirken bazıları daha etkisiz hale dönüşmektedir. Amaç, ilacı daha suda çözünür hale getirerek atılımını kolaylaştırmaktır. Atılım (eliminasyon) ilacın ve metabolitlerinin vücuttan uzaklaştırılmasıdır. En yaygın yol böbrekler (idrar) olsa da safra, ter, tükürük ve akciğerler de atılım sürecinde rol oynar. Pharmacokinetics is the branch of science that examines what the body does to a drug. Fundamentally, it consists of four principal processes: absorption, distribution, metabolism (biotransformation), and excretion (elimination), collectively referred to by the acronym ADME. Absorption is the process by which a drug enters the systemic circulation from its site of administration, such as oral, parenteral, or dermal routes. The rate of absorption varies depending on numerous factors. Distribution refers to the dissemination of the drug to tissues through the bloodstream. In this process, factors such as plasma protein binding, tissue affinity for the drug, and the blood–brain barrier play significant roles. The volume of distribution (Vd) indicates the extent to which a drug disperses throughout the body. Metabolism (biotransformation) involves the chemical alteration of a drug, primarily in the liver. Enzymes, particularly those of the cytochrome P450 system, play a crucial role in this process. While some drugs are converted into more active forms, others become less active. The primary objective of metabolism is to increase the water solubility of the drug, thereby facilitating its excretion. Excretion (elimination) is the removal of the drug and its metabolites from the body. Although the kidneys (via urine) constitute the most common route of excretion, bile, sweat, saliva, and the lungs also contribute to the elimination process.