Histochemical and immunohistochemical investigation of the number and localization of mast cells in the feline tongue.

This is the first study to describe the subtypes, number and distribution of mast cells (MC) in cat tongue by histochemical and immunohistochemical methods. Six male adult felines' tongue tissue samples consist of the study's material. Samples were fixed in 10% formaldehyde. MC number and distribution in the feline tongue were assessed using toluidine blue. Also, sections taken from blocks were stained in alcian blue/safranin O (AB/SO) combined dyes to determine the MC subtypes. The Streptavidin biotin complex method using anti-chymase and anti-tryptase primary antibodies was used for immunohistochemistry. Metachromatic MCs were mainly observed in the lamina propria close to the multilayered keratinized stratified squamous epithelium. The high number of MCs in this region may be because the dorsal surface of the tongue plays an essential role in the defence system of tongue tissue and, thus, of the body as a whole. Additionally, the number of MCs stained with AB (+) (1.7 ± 0.08) in the feline tongue was statistically higher than those with SO (+) (0.18 ± 0.02). This might be interpreted as an indication that MC heterogeneity may be due not only to their staining properties but also to their localization. It is also conceivable that the high histamine content may be a factor in this. Tryptase-positive MCs were found in the loose connective tissue around blood vessels, between the glands, as solitary cells, or in groups of several cells. Chymase-positive MCs were observed more individually rather than in groups. Moreover, chymase-positive MCs were detected to be located in the filiform papillae subepithelial and in the blood vessels' immediate vicinity. Animals often lick themselves to clean themselves and promote healing. For this reason, it is very important to protect the tongue, which is in direct contact with the external environment, against foreign agents. Considering both the functional and protective properties of the tongue, we concluded that MCs may play a role in oral cavity immunity and protective effect.

Targeting Aquaporin-5 by Phosphodiesterase 4 Inhibition Offers New Therapeutic Opportunities for Ovarian Ischemia Reperfusion Injury in Rats.

This study aimed to examine the effect of Phosphodiesterase 4 (PDE4) inhibition on Aquaporin-5 (AQP5) and its potential cell signaling pathway in the ovarian ischemia reperfusion (OIR) model. Thirty adult female rats were divided into five groups: Group 1; Control: Sham operation, Group 2; OIR that 3 hour ischemia followed by 3 hour reperfusion, Group 3; OIR + Rolipram 1 mg/kg, Group 4; OIR + Rolipram 3 mg/kg, Group 5; OIR + Rolipram 5 mg/kg. Rolipram was administered intraperitoneally to the rats in groups 3-4 and 5 at determined doses 30 minutes before reperfusion. From ovary tissue; Tumor necrosis factor-a (TNF-α), Cyclic adenosine monophosphate (cAMP), Nuclear factor kappa (NF-κB), Interleukin-6 (IL-6), Phosphodiesterase 4D (PDE4D), Mitogen-activated protein kinase (MAPK) and AQP5 levels were measured by ELISA. We also measured the level of AQP5 in ovary tissue by real-time reverse-transcription polymerase chain reaction (RT-PCR). In the OIR groups; TNF-α, NF-κB, IL-6, MAPK inflammatory levels increased, and cAMP and AQP5 levels decreased, which improved with the administration of rolipram doses. Also histopathological results showed damaged ovarian tissue after OIR, while rolipram administration decrased tissue damage in a dose dependent manner. We propose that the protective effect of PDE4 inhibition in OIR may be regulated by AQP5 and its potential cell signaling pathway and may be a new target in OIR therapy. However, clinical studies are needed to appraise these data in humans.

Effect of trimetazidine against ovarian ischemia/reperfusion injury in rat model: A new pathway: JAK2/STAT3.

Objectives: Ovarian ischemia/reperfusion (I/R) is an extremely complex pathological problem that begins with oxygen deprivation, progresses to excessive free radical production, and intensifies inflammation. The JAK2/STAT3 signaling pathway is a multipurpose signaling transcript channel that plays a role in several biological functions. Trimetazidine (TMZ) is a cellular anti-ischemic agent. This study aims to investigate the effects of TMZ on ovarian I/R injury in rats. Materials and Methods: sixty four rats were divided into 8 groups at random: healthy(group1); healthy+TMZ20(group2); ischemia (I) (group 3); I+TMZ10(group4); I+ TMZ20(group5); I/R(group6); I/R+TMZ10(group7); I/R+TMZ20(group8). Vascular clamps were placed just beneath the ovaries and over the uterine horns for 3 hr to induce ischemia. The clamps were removed for the reperfusion groups, and the rats were reperfused with care to ensure that the blood flowed into the ovaries, subjecting them to reperfusion for 3 hr. TMZ was administered orally by gavage 6 and 1 hr before operations. At the end of the experiment, ovarian tissues were removed for biochemical, molecular, and histopathological investigation. Results: TMZ administration ameliorated ischemia/reperfusion-induced disturbances in GSH and MDA levels. TMZ treatment inhibited I/R-induced JAK2/STAT3 signaling pathway activation in ovarian tissues. TMZ administration also improved the increase in the mRNA expressions of IL-1ß, TNF-α, and NF-κB caused by ischemia/reperfusion injury. Moreover, TMZ treatment improved histopathologic injury in ovarian tissues caused by ischemia/reperfusion. Conclusion: TMZ treatment protected rats against ovarian ischemia/reperfusion injury by alleviating oxidative stress and inflammatory cascades. These findings may provide a mechanistic basis for using TMZ to treat ovarian ischemia-reperfusion injury.

Protective effects of a natural product, paeoniflorin, on ischemia reperfusion injury on rat ovary tissue: histopathological, immunohistochemical, and biochemical study.

In this study, the main hypothesis is that paeoniflorin may inhibit some cellular processes such as oxidative stress and inflammation. For this reason, we aimed to investigate the potential protective effects of a natural compound, paeoniflorin, on rat model of ovarian ischemia-reperfusion injury by detecting the oxidative stress parameters and inflammatory process parameters. 42 female Wistar-albino rats were divided into 6 random groups. The rats were subjected to 3-hour ischemia and 3-hour reperfusion process. Then, paeoniflorin at doses of 25, 50 and 100 mg/kg were applied 30 min before the reperfusion. The levels of pro-inflammatory (IL-1-ß, IL-6, TNF-α) and anti-inflammatory (IL-10, TGF-ß) cytokines were measured by ELISA. Similarly, IL-6, IL-10, TNF-α, NF-κB p65) positivity rates were detected by immunohistochemical staining. Additionally, oxidative stress parameters (MDA, GSH, SOD) were measured by tissue biochemistry. Ischemia-reperfusion injury caused significant increase in the levels of SOD, MDA, TNF-α, IL-1-ß, IL-6 and NF-κB p65, while paeoniflorin treatments improved the related parameters in a dose-dependent manner. As a conclusion, our findings support the evidence that paeoniflorin has a potential protective effects on ovarian ischemia-reperfusion injury. Further detailed studies should be performed to shed light the molecular mechanism of these protective effects.

The effects of cisplatin and jaceosidin on SH-SY5Y neuroblastoma cells: an electron microscopic, molecular and biochemical study.

In this study, our aim was to show both the single and combined effects of cisplatin and jaceosidin in SHSY-5Y neuroblastoma cells. For this purpose, we used MTT cellular viability assay, Enzyme-Linked Immunosorbent Assay (ELISA), Transmission Electron Microscopy (TEM), Immunofluorescence Staining Assay (IFA) and Western blotting (WB) assay. According to MTT findings, IC50 dose was detected as 50 µM cisplatin and 160 µM jaceosidin co-application. Therefore, experimental groups were finally selected as control, cisplatin, 160 µM jaceosidin and Cisplatin +160 µM jaceosidin. Cell viability was decreased in all groups, and the IFA findings confirmed the viability analysis. WB data indicated that matrix metalloproteinase 2 and 9 levels, as indicators of metastasis, decreased. While LPO and CAT levels increased in all treatment groups, it was observed that the activity of SOD decreased. When TEM micrographs were investigated, cellular damages were determined. In the light of these results, it can be said that cisplatin and jaceosidin have a potential to increase the effects of each other synergistically.

Two flavonoids, baicalein and naringin, are effective as anti-inflammatory and anti-oxidant agents in a rat model of polymicrobial sepsis.

INTRODUCTION: In this study, our aim was to investigate the possible protective and therapeutic effects of these two flavonoids, baicalein, and naringin, in 50 and 100 mg/kg doses applied both before and after cecal ligation and puncture (CLP) procedures in a polymicrobial sepsis rat model, and evaluate the possible contribution of oxidative and inflammatory markers by immunological, biochemical, molecular, and histopathological methods. METHODS: Sixty-six Wistar albino rats were divided into 11 groups. The pro-inflammatory (TNF-alpha, IL-1-beta, and IL-6) and anti-inflammatory (TGF-beta and IL-10) cytokine levels were measured by ELISA technique. CD3, CD68, and nuclear factor kappa B positivity rates were detected by immunohistochemical methods. Oxidative stress parameters (MDA, SOD, and GSH) were measured by tissue biochemistry. RESULTS: Sepsis caused a significant increase in all pro-inflammatory cytokine levels and MDA activity. Also, it led to an increase in the positivities of CD3, CD68, and NF-κB markers. However, especially pre-CLP doses of baicalein and naringin inhibited the inflammation process by suppressing pro-inflammatory and increasing anti-inflammatory cytokine levels, as well as regulating the oxidative stress process by normalizing the oxidant/anti-oxidant enzyme levels. CONCLUSION: Both pre- and post-application of baicalein and naringin are quite effective to prevent sepsis-caused cellular processes. This protective and therapeutic effects by baicalein and naringin in animals with sepsis seems to be originated from the high antioxidant capacity and inhibition of pro-inflammatory cytokine production. Thus, those natural agents may prove to be valuable protective agent against septic shock.

Benefits of Some Phytochemical Compounds in Experimental Sepsis Models: A Therapeutic Perspective.

Sepsis represents a major contributor to mortality among critically ill patients, imposing a substantial economic strain on health-care systems. The uncontrolled inflammatory response during sepsis development, often leading to multiorgan failure and death, remains a challenge despite advances in antibiotics and supportive care. Factors such as antibiotic resistance, noninfectious causes, and delays in treatment initiation contribute to the complexity of managing sepsis. This review explores alternative treatment strategies focusing on the ameliorative efects of widely consumed phytochemicals and their cellular and molecular mechanisms in various in vitro and in vivo sepsis models. Preemptive administration of phytochemicals before sepsis onset appears efective, emphasizing their potential as adjunct or complementary therapeutic agents for critically ill sepsis patients. As a consequence, phytochemicals can be included in treatment regimens to enhance overall efectiveness and expedite the healing process.