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.

Preterm birth remains a major contributor to neonatal morbidity, primarily due to immature lung development and insufficient surfactant production. Although antenatal corticosteroids (ACS) are widely used to accelerate fetal lung maturation, concerns regarding their potential systemic effects have prompted the search for alternative or adjunctive agents. Erdosteine, a thiol-based compound with anti-inflammatory and antioxidant properties, may represent a promising candidate. Pregnant Sprague–Dawley rats were randomly assigned to four groups ( n = 6 dams per group): control, dexamethasone (DEX), betamethasone (BET), and erdosteine (ERDO). All treatments were administered antenatally to the pregnant dams via intraperitoneal injection. DEX and BET were given on gestational days (GD) 16–18, while ERDO was administered on GD16–20. Preterm delivery was achieved by cesarean section on GD20. Lung tissues of pups born to treated dams were collected on postnatal day 5 (P5) and analyzed using histopathological and immunohistochemical methods, including Caspase-3, PCNA, ABCA3 (ATP-binding cassette subfamily A member 3), SFTPA1, AQP5, and SP-B. DEX and BET groups demonstrated lung architecture consistent with accelerated maturation, whereas ERDO preserved alveolar structure with only mild interstitial inflammation. Caspase-3 and PCNA expression were markedly increased in corticosteroid-treated groups but remained low in ERDO and control groups. Notably, ABCA3 expression was highest in the ERDO group across both compartments ( p < 0.001). SFTPA1 expression was also more prominent in the interstitial compartment in the ERDO group. AQP5 and SP-B showed no significant expression in any group. Erdosteine demonstrated a biologically favorable profile characterized by reduced inflammatory response, preservation of lung architecture, and enhanced expression of key surfactant-related markers, particularly ABCA3. While not fully replicating the effects of antenatal corticosteroids, its anti-inflammatory and antioxidant properties suggest that it may serve as a supportive or complementary strategy for promoting fetal lung maturation. Further experimental and translational studies are warranted.

Peritonit çok sık olarak karşımıza çıkan karın duvarında ki enfeksiyonla karakterize bir hastalıktır. Yaygın olarak görülmesine ve karmaşık bir patofizyolojik sürece sahip olduğundan dolayı bu karmaşık süreci açıklığa kavuşturmak amacıyla deney hayvan modelleri geliştirilmiştir. Bu modeller arasında sekum ligasyon ve punksiyon (Cecal Ligation and Puncture; CLP) modeli, ratlarda polimikrobiyal peritonit ve devam eden süreçte sepsis oluşturmak için kullanılan en geçerli ve klinik olarak en fazla kabul gören deneysel yöntemdir. Bu yöntemin doğal olarak vücutta bulunan sekum florası ile oluşturabiliyor olması, yapılan ligatür ve punksiyona bağlı olarak farklı şiddetlerde peritonitis oluşmasının sağlanabilmesi gibi üstünlükleri olup klinik olarak görülen peritonit vakalarıyla paralellik göstermektedir. Doğru anatomik yaklaşımla sekumun belirli bir bölümünün ligasyonu ve uygun kalınlıkta bir iğne ile delinmesiyle fekal içerik sızıntısı oluşturarak doğal enfeksiyon süreci başlatılmış olur. Bu model, proinflamatuvar sitokin artışı, bakteriyemi, hemodinamik bozulma ve organ disfonksiyonu gibi sepsisin karakteristik özelliklerini benzer biçimde taklit eder. Bu nedenle CLP, peritonit, sepsis patofizyolojisini incelemek ve yeni tedavi seçeneklerini test etmek için “altın standart” preklinik model olarak kabul edilmektedir. Peritonitis is a disease characterized by frequent infection of the abdominal wall. Due to its common occurrence and complex pathophysiological process, animal models have been developed to elucidate this complex process. Among these models, the Cecal Ligation and Puncture (CLP) model is the most valid and clinically accepted experimental method used to induce polymicrobial peritonitis and subsequent sepsis in rats.This method has several advantages, such as being able to induce infection using the naturally occurring cecal flora of the body and allowing for peritonitis of varying severity depending on the ligature and puncture performed, which parallels clinically observed peritonitis cases. By achieving the correct anatomical approach, the natural infection process is initiated by ligating a specific portion of the cecum and puncturing it with an appropriately sized needle to create a leakage of fecal contents. This model reliably mimics the characteristic features of sepsis, such as an increase in pro-inflammatory cytokines, bacteremia, hemodynamic derangement, and organ dysfunction. For this reason, CLP is accepted as the "gold standard" preclinical model for studying the pathophysiology of peritonitis and sepsis and for testing new therapeutic options.

Deneysel testis torsiyonu modeli, testisin kendi vertikal ekseni boyunca dönerek testis dokusunun iskemi altında kalmasını simüle etmek için kullanılan bir yöntemdir. Bu model, testisin gençlerde ve erginlerdeki torsiyonunu deney hayvanlarında oluşturarak testis iskemisi/reperfüzyonunun hasar mekanizmlarını araştırmaya olanak sağlayan elverişli bir modeldir. 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. Dokunun yeniden kanlanmaya başladığı reperfüzyon aşaması paradoksal olarak hipoksik hasarın düzeyinin şiddetlendiği aşamadır. Bu aşamada dokunun aniden yeniden kanlanması ve oksijenizasyon dokudaki inflamatuar süreçleri tetikleyerek hücresel hasarı artırmaktadır. The experimental testicular torsion model is a methodology utilized to simulate the ischemic injury sustained by testicular tissue as a result of the testis rotating along its vertical axis. This model is highly suitable for investigating the underlying damage mechanisms of testicular ischemia/reperfusion (IR) in both juvenile and adult experimental subjects. Ischemia is defined as the mechanical restriction of arterial, venous, or combined blood flow to a specific tissue. The severity of the resulting damage is contingent upon the duration of the ischemia, the degree of restriction, and the anatomical site of the obstruction. The subsequent reperfusion phase, which involves the reintroduction of blood flow, paradoxically represents the stage where the extent of hypoxic damage is exacerbated. During this phase, the sudden reoxygenation and reperfusion of the tissue trigger robust inflammatory processes, thereby amplifying cellular injury.

Lead (Pb), a pervasive environmental pollutant, has been linked to various reproductive health issues, including infertility and hormonal imbalances. Species of Astragalus, renowned for their antioxidant and anti-apoptotic properties, may mitigate these adverse effects by promoting folliculogenesis and restoring hormone levels disrupted by Pb exposure. In this study, the protective potential of astragalus polysaccharides (APS) against lead induced ovarian toxicity was investigated, both when administered alone and in combination with vitamin E and selenium. The aim was to determine whether the observed protective effects are linked to the antioxidant capacity of APS, and to explore the possible contribution of its anti-apoptotic properties. Thirty-six female Wistar rats (220-250 g) were divided into treatment groups and administered lead, APS, vitamin E, and selenium for a duration of 15 days. Estradiol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and antioxidant levels were measured at the end of the study. Additionally, ovarian tissue damage and apoptosis were assessed through immunohistochemistry. The results indicated that Pb induced reductions in hormone levels were significantly restored to near control levels in the APS treated groups. Moreover, antioxidant levels were notably elevated in these groups. Immunohistochemical analysis revealed a significant reduction in stromal and follicular degeneration in the ovaries of rats treated with APS. In conclusion, APS, both independently and in combination with vitamin E and selenium, exhibited substantial protective effects against Pb induced ovarian toxicity.