Protective Effect of Ramipril Against Oxidant and Proinflammatory Cytokine Damage Induced by Ischemia-Reperfusion in Ovarian Tissue in Rats.

BACKGROUND: It is known that the increase in oxidants and proinflammatory cytokines, as well as the decrease in antioxidants, play a role in ovarian ischemia-reperfusion (I/R) injury. The antioxidant and anti-inflammatory properties of ramipril have been studied in various diseases. This study aims to investigate the effect of ramipril on I/R-induced ovarian damage in rats. METHODS: Rats were divided into healthy (HG), sham (SG), ovary I/R (OIR), and ramipril + ovary I/R (ROIR) groups (n = 6/each group). One hour before the surgical procedures, ROIR was given 2 mg/kg ramipril. The lower abdomen of the SG, OIR, and ROIR was surgically opened. Right ovarian tissues of OIR and ROIR were subjected to 2 hours of ischemia and 6 hours of reperfusion. Then, all animals were euthanized, and their right ovaries were removed. Ovarian tissues were examined for oxidants (malondialdehyde), antioxidants (total glutathione, superoxide dismutase, and catalase), and proinflammatory cytokines (nuclear factor kappa-B, tumor necrosis factor-alpha, interleukin 1 beta, and interleukin-6) analysis was performed. Tissues were examined histopathologically. RESULTS: The ovarian tissue of the OIR, which underwent the I/R procedure, exhibited a significant increase in oxidant and proinflammatory cytokine levels, along with a decrease in antioxidant levels (P < .001). Ramipril suppressed the I/R-induced increase in oxidants and pro-inflammatory cytokines and the decrease in antioxidants (P < .001). Ramipril also attenuated I/R-induced histopathological damage in ovarian tissue (P < .05). CONCLUSION: Ramipril treatment may be a treatment strategy to protect ovarian tissue against oxidative and inflammatory damage of I/R.

Effects of taxifolin on tramadol-induced oxidative and inflammatory liver injury in rats: an experimental study.

In this experimental study we aimed to investigate the biochemical and histopathological effects of concomitantly administered taxifolin on tramadol-induced liver damage in rats. The rats were divided into three groups; control group (CG), tramadol alone (TRG), and taxifolin + tramadol given (TTRG) groups. Malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS), total antioxidant status (TAS), nuclear factor-kappa beta (NF-kB), tumor necrosis factor-α (TNF-α), and interleukin-1ß (IL-1ß) levels were measured in liver tissues. Liver tissues were also examined histopathologically. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were determined in blood samples. In tissue analyses, determinants of oxidative stress and inflammation, all were significantly higher in the TRG group compared with the control and TTRG groups. In the TTRG group, all oxidative stress and inflammation markers were significantly lower than in the TRG group. In addition, there was not any significant difference between the control and TTRG groups regarding the TOS and TAS status. Serum liver enzymes were also significantly higher in the TRG group than in the other two groups. In histopathological examinations, the control group had a normal histological appearance. Degenerative-necrotic hepatocytes and hemorrhage, which were seen at a severe level in the TRG group, were found to be moderate in the treated TTRG group. In addition, mononuclear cell infiltrations were found to be severe in the TRG group and mild in the treated TTRG group. Finally it was concluded that Taxifolin alleviated the toxic effects of tramadol on the liver including the histopathological and biochemical changes as well as the oxidative damage.

Carvacrol prevents acrylamide-induced oxidative and inflammatory liver damage and dysfunction in rats.

Background: Acrylamide causes hepatotoxicity with the effect of oxidative stress and inflammatory processes. Carvacrol is a monoterpenic phenol with antioxidant and anti-inflammatory properties. Aims: To determine the effects of carvacrol on oxidative liver injury induced by acrylamide administration in rats. Methods: Rats were divided into three groups of six animals each: healthy group acrylamide group (ACR), and acrylamide + carvacrol group (TACR). First, carvacrol (50 mg/kg) was administered intraperitoneally to the CACR group. One hour later, acrylamide (20 mg/kg) was given orally to the ACR and CACR groups. This procedure was performed for 30 days, after which the animals were sacrificed. The malondialdehyde (MDA) and total glutathione (tGSH) levels, total oxidant (TOS) and total antioxidant status (TAS), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1ß), and nuclear factor kappa b (NF-κB) were measured in the excised liver tissues. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were determined in blood serum samples. Liver tissues were also examined histopathologically. Results: In the ACR group, malondialdehyde, TOS, ALT, AST levels, and NF-κB, IL-1ß, and TNF-α levels were found to be high, and tGSH and total antioxidant status levels were low. In addition, diffuse degenerative changes and necrosis in hepatocytes, and moderate inflammation in the portal region were detected in the liver tissues of the ACR group. While carvacrol prevented the biochemical changes induced by acrylamide, it also alleviated the damage in the histological structure. Conclusion: Carvacrol may be used for liver damage caused by acrylamide.

The effect of carvacrol on the proinflammatory cytokines, histology, and fertility outcome of cisplatin-related ovarian change in a rat model.

OBJECTIVE: In women, agents used in chemotherapy treatment have side effects such as accelerating follicular depletion and early menopause. Thus, cytotoxic treatments may cause various effects ranging from partial damage to the ovary to premature ovarian failure (POI) and infertility. This study aimed to investigate the protective effect of carvacrol on cisplatin (CIS)-induced reproductive toxicity in female rats. MATERIALS AND METHODS: The animals were divided to four groups; a healthy group (HG), administered only cisplatin 2.5 mg/kg (CIS); cisplatin 2.5 mg/kg + carvacrol mg/kg (CC-50), and cisplatin 2.5 mg/kg + carvacrol 100 mg/kg (CC-100). In this study, the CC-50 and CC-100 groups were injected with carvacrol at 50 and 100 mg/kg intraperitoneally (IP). The CIS and HG groupswere administered normal saline as a solvent in the same way. One hour afterwardthe CC-50 and CC-100 groups were injected with cisplatin at 2.5 mg/kg IP. This procedure was continued once a day for 14 days. At the end of this period, six rats from each group were euthanized with high-dose anaesthesia. Biochemical (oxidant-antioxidant and proinflammatory cytokines) and histopathological examinations were performed on the right ovarian tissue removed from the dead rats. The remaining (n = 6 in each group) animals were kept in the laboratory with mature male rats for two months for breeding. Rats that didn't give birth within two months were considered infertile. A one-way ANOVA test was used for the biochemical analysis, the a Kruskal Wallis test was used for the histopathological analysis. RESULTS: It has been observed that cisplatine causes oxidative stress and inflammatory damage in the ovarian tissue of animals and ultimately causes infertility due to this oxidative stress. While carvacrol significantly suppressed cisplatin-related oxidative stress in ovarian tissue at the 50 and 100 mg/kg doses, it could suppress proinflammatory cytokine increase only at thecytokine increase only at the 100 mg/kg dose. In addition, carvacrol significantly reduced the development of cisplatin-related infertility (from 0 to 83.3%) at a dose of 100 mg/kg. CONCLUSION: These findings suggest that carvacrol at high doses can reduce the harmful effects of cisplatin on the ovary and improve ovarian reserve in rats.

Effects of benidipine, paracetamol, and their combination on postoperative and normal tissue pain thresholds.

Introduction: In clinical practice, inadequate pain inhibition leads to increased morbidity and mortality. Increased intracellular calcium, oxidants, and proinflammatory cytokines are known to play a role in the pathogenesis of postoperative pain. Therefore, we investigated the analgesic effects of benidipine, paracetamol, and benidipine-paracetamol combination (BPC) on postoperative and normal pain thresholds in rats. Material and methods: Sixty-four male albino Wistar rats weighing 285-295 g were used. The without-incision rats were divided into 4 subgroups: healthy control, benidipine alone, paracetamol alone, and BPC. The scalpel-incision rats were divided into 4 subgroups: scalpel incision, scalpel incision + benidipine, scalpel incision + paracetamol, and scalpel incision + BPC. Paw pain thresholds of rats were measured using a Basile algesimeter. Biochemical analyses were performed on the paw tissues of 6 rats randomly taken from the experimental groups, each containing 8 rats. Rats were sacrificed immediately after the measurements. After the pain threshold tests were finished, the paw tissues were removed and malondialdehyde (MDA), total glutathione (tGSH), cyclooxygenase (COX), and interleukin-6 (IL-6) levels were measured. Results: There was no significant difference between the groups in paw pain threshold and measured biochemical parameters in rats without incision. The decrease in the pain threshold of the incised paw was also best prevented by BPC, followed by benidipine and then paracetamol. Furthermore, increases in scalpel-incised paw tissue MDA, COX-2, and IL-6 levels and the decrease in tGSH were significantly suppressed by benidipine and BPC, while paracetamol could only significantly inhibit the increase in IL-6 production. Conclusion: The combination of the L-type Ca2+ channel blocker benidipine and paracetamol (BPC) may provide potent analgesia. Our experimental results support that BPC may be useful in the treatment of severe pain that cannot be adequately inhibited by paracetamol.

The effect of rutin on pulmonary contusion induced by blunt trauma in rats: Biochemical and histopathological evaluation.

Background: This study aims to investigate the possible protective effects of rutin, also called vitamin P1, against pulmonary contusion induced by blunt chest trauma in a rat model. Methods: Thirty male albino Wistar rats were separated into three equal groups as healthy group, trauma group, and trauma+rutin group. After anesthesia provided by intraperitoneal administration of 60 mg/kg ketamine and xylazine by inhalation at appropriate intervals, 200 g weight was dropped from 1 m height to the anterior chest wall of the animals in the trauma group (n=10) and trauma+rutin group (n=10) and pulmonary contusion was created. Thirty min after the trauma, 50 mg/kg of rutin was administered into the stomach of trauma+rutin group animals orally with gavage. The rats received rutin once daily for two days and were sacrificed 48 h later. Their lung tissues were removed and examined biochemically and histopathologically. Results: Nuclear factor-kappa B, cyclooxygenase-2, and malondialdehyde levels increased in the trauma group compared to the healthy group, and rutin administration prevented this increase. Total glutathione levels decreased in the trauma group, and rutin administration also prevented this decrease. The histopathological findings were compatible with the biochemical findings. Conclusion: Our study results suggest that rutin has a protective effect on contused lung tissue in rats.

The effect of taxifolin on oxidative sciatic nerve damage induced by cobalt chloride in rats: a biochemical and histopathological evaluation.

Cobalt is a trace element that increases lipid peroxidation and malondialdehyde levels and reduces the antioxidant defense mechanisms of nerve cells. High levels of cobalt exposure may cause peripheral neuropathy, but the mechanism behind this has not yet been elucidated. Taxifolin is a flavonoid whose antioxidant and anti­inflammatory properties are well­known. We aimed to investigate the effect of taxifolin on cobalt­induced oxidative sciatic nerve damage. Eighteen albino male Wistar rats were assigned to three groups: Control, Cobalt, and Taxifolin + Cobalt groups. Total oxidant and total antioxidant status and levels of malondialdehyde, total glutathione, and superoxide dismutase were measured to determine the effect of taxifolin on cobalt­induced sciatic nerve injury. The following statistically significant effect of taxifolin was observed: It prevented cobalt­induced oxidative sciatic nerve damage by reducing malondialdehyde levels and total oxidant status and increasing total antioxidant status, total glutathione levels, and superoxide dismutase levels. In a histopathological analysis, we observed similar findings in Control and Taxifolin + Cobalt groups. We determined that taxifolin is effective in preventing cobalt­induced oxidative damage in sciatic nerve injury.

Effect of taxifolin on methotrexate-induced oxidative and inflammatory oral mucositis in rats: biochemical and histopathological evaluation.

BACKGROUND: The role of oxidative stress, as well as inflammation in the pathogenesis of methotrexate (MTX)-induced oral mucositis, is a known fact. The anti-inflammatory, antitumor, antimicrobial, and antioxidant properties of taxifolin-the effect we tested against MTX-induced oral mucosal damage-are well known. OBJECTIVE: Evaluating biochemically and histopathologically the effects of taxifolin on methotrexate-induced oral mucosal damage in rats. METHODOLOGY: In the taxifolin+MTX (TMTX) group, 50 mg/kg taxifolin was orally administered to rats by gavage. In the MTX and healthy (HG) groups, normal saline was applied to rats as solvent by the same method. One hour after administration of taxifolin and solvent, 5 mg/kg MTX was orally administered to rats in the MTX and TMTX groups. Taxifolin and methotrexate were administered once a day for 30 days. Macroscopic, biochemical, and histopathological evaluations were performed on the inner cheek and tongue tissues of rats. These parts were removed after rats were killed with a high-dose anesthesia. RESULTS: Taxifolin with MTX prevented the increase in oxidant and pro-inflammatory parameters, such as malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1ß), interleukin 6 (IL-6), on the inner cheek and tongue tissues of rats. Moreover, taxifolin antagonized the decrease in total glutathione (tGSH). Taxifolin decreased MTX-induced histopathological damage. CONCLUSION: These findings suggest that taxifolin may be useful to treat MTX-associated oral mucositis.

Amelioration of oxidative damage parameters by carvacrol on methanol-induced liver injury in rats.

The methanol metabolite that causes hepatotoxicity is formic acid, generating reactive oxygen radical formation and cell damage. Carvacrol is an antioxidant monoterpenic phenol produced from Thymus vulgaris. This study aimed to investigate the effects of carvacrol on methanol-induced oxidative liver damage in rats. Eighteen rats were divided into three groups. Methotrexate was administered orally for 7 days to methotrexate+methanol (MTM) and methotrexate+methanol+carvacrol (MMC) groups. Methotrexate was given before methanol to cause methanol poisoning. Distilled water was given to the healthy group (HG) as a solvent. At the end of the 7th day, 20% methanol was administered orally at a dose of 3 g/kg to the MTM and MMC groups. Four hours after methanol administration, 50 mg/kg carvacrol was injected intraperitoneally into the MMC group. Animals were sacrificed 8 h after carvacrol injection. Biochemical markers were studied in the excised liver tissue and blood serum samples, and histopathological evaluations were made. Severe hemorrhage, hydropic degeneration, pycnosis, and mononuclear cell infiltration were observed in the liver of the MTM group. Additionally, the levels of malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly higher, and total glutathione (tGSH) and total antioxidant status (TAS) were significantly lower in the MTM group compared to HG (P<0.001). Carvacrol prevented the increase in MDA, TOS, ALT and AST levels with methanol and the decrease in tGSH and TAS levels (P<0.001), and alleviated the histopathological damage. Carvacrol may be useful in the treatment of methanol-induced liver damage.

COVID-19 is more dangerous for older people and its severity is increasing: a case-control study.

Coronavirus disease 2019 (COVID-19) triggers important changes in routine blood tests. In this retrospective case-control study, biochemical, hematological and inflammatory biomarkers between March 10, 2020, and November 30, 2020 from 3969 COVID-19 patients (3746 in the non-intensive care unit (non-ICU) group and 223 in the ICU group) were analyzed by dividing into three groups as spring, summer and autumn. In the non-ICU group, lymphocyte to monocyte ratio was lower in autumn than the other two seasons and neutrophil to lymphocyte ratio was higher in autumn than the other two seasons. Also, monocyte and platelet were higher in spring than autumn; and eosinophil, hematocrit, hemoglobin, lymphocyte, and red blood cells decreased from spring to autumn. In the non-ICU group, alanine aminotransferase and gamma-glutamyltransferase gradually increased from spring to autumn, while albumin, alkaline phosphatase, calcium, total bilirubin and total protein gradually decreased. Additionally, C-reactive protein was higher in autumn than the other seasons, erythrocyte sedimentation rate was higher in autumn than summer. The changes in routine blood biomarkers in COVID-19 varied from the emergence of the disease until now. Also, the timely changes of blood biomarkers were mostly more negative, indicating that the disease progresses severely. The study was approved by the Erzincan Binali Yildirim University Non-interventional Clinical Trials Ethic Committee (approval No. 86041) on June 21, 2021.

Effect of taxifolin on methotrexate-induced oxidative and inflammatory oral mucositis in rats: biochemical and histopathological evaluation

Abstract The role of oxidative stress, as well as inflammation in the pathogenesis of methotrexate (MTX)-induced oral mucositis, is a known fact. The anti-inflammatory, antitumor, antimicrobial, and antioxidant properties of taxifolin—the effect we tested against MTX-induced oral mucosal damage—are well known. Objective Evaluating biochemically and histopathologically the effects of taxifolin on methotrexate-induced oral mucosal damage in rats. Methodology In the taxifolin+MTX (TMTX) group, 50 mg/kg taxifolin was orally administered to rats by gavage. In the MTX and healthy (HG) groups, normal saline was applied to rats as solvent by the same method. One hour after administration of taxifolin and solvent, 5 mg/kg MTX was orally administered to rats in the MTX and TMTX groups. Taxifolin and methotrexate were administered once a day for 30 days. Macroscopic, biochemical, and histopathological evaluations were performed on the inner cheek and tongue tissues of rats. These parts were removed after rats were killed with a high-dose anesthesia. Results Taxifolin with MTX prevented the increase in oxidant and pro-inflammatory parameters, such as malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), on the inner cheek and tongue tissues of rats. Moreover, taxifolin antagonized the decrease in total glutathione (tGSH). Taxifolin decreased MTX-induced histopathological damage. Conclusion These findings suggest that taxifolin may be useful to treat MTX-associated oral mucositis.

The Effect of Anakinra on Acrylamide-induced Peripheral Neuropathy and Neuropathic Pain in Rats

Abstract Acrylamide is a neurotoxic compound. Moreover, anakinra is an interleukin-1 (IL-1) receptor antagonist used in rheumatoid arthritis treatment. This study investigated the effect of anakinra on acrylamide-related neuropathy and neuropathic pain. Acrylamide exposure caused a significant decrease in the pain threshold; an increase in malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1ß) levels; and a decrease in total glutathione (tGSH) values in the sciatic nerve. This indicates hyperalgesia presence, oxidative stress, and peripheral nerve tissue inflammation. Anakinra treatment significantly reduced the MDA, IL-1ß, and TNF-α levels, and increased the pain threshold and mean tGSH values. The analgesic effect of anakinra was 67.9% at the first hour, increasing to 74.9% and 76.7% at the second and third hours, respectively. The group receiving acrylamide exhibited histopathological changes (e.g., swollen and degenerated axons, hypertrophic and hyperplasic Schwann cells, and congested vessels). The use of anakinra significantly improved these morphological changes. Anakinra is concluded to reduce neuropathic pain and prevent neurotoxic effect of acrylamide on peripheral nerves due to its analgesic, antioxidant, and anti-inflammatory properties

Effect of adenosine triphosphate, benidipine and their combinations on bevacizumab-induced kidney damage in rats.

BACKGROUND: Bevacizumab-induced vascular endothelial growth factor (VEGF) inhibition may lead to a decrease in adenosine triphosphate (ATP) levels, an increase in intracellular Na+ and Ca2+ concentrations and an increase in reactive oxygen species (ROS) generation, as well as to cell damage. OBJECTIVES: To investigate the biochemical and histopathological effects of ATP, benidipine and ATP in combination with benidipine on bevacizumab-induced kidney damage in rats. MATERIAL AND METHODS: Rats were divided into 5 treatment groups: bevacizumab (BVZ) alone, ATP + bevacizumab (ABVZ), benidipine + bevacizumab (BBVZ), ATP + benidipine + bevacizumab (ABBVZ), and healthy controls (HC). Adenosine triphosphate (25 mg/kg), benidipine (4 mg/kg orally), ATP (25 mg/kg) + benidipine (4 mg/kg), or saline were administered to albino Wistar rats. One hour after treatment, bevacizumab was injected at a dose of 10 mg/kg to induce kidney damage. Two doses of bevacizumab were delivered 15 days apart. Adenosine triphosphate + benidipine were administered once a day for 1 month. RESULTS: Malondialdehyde (MDA), total oxidant status (TOS), creatinine, and blood urea nitrogen (BUN) levels of the BVZ, BBVZ, ABVZ, ABBVZ, and HC groups were ranked from highest to lowest. Conversely, total glutathione (tGSH) and total antioxidant status (TAS) kidney tissue values were ranked from lowest to highest, respectively. Hemorrhage, tubular necrosis and grade 3 focal tubular atrophy were observed in the BVZ group. Atrophy and grade 2 necrosis were observed in the BBVZ group and atrophy and grade 1 necrosis were observed in the ABVZ group. Only grade 1 atrophy was observed in the ABBVZ group. CONCLUSIONS: Adenosine triphosphate reduced bevacizumab-induced renal toxicity significantly more effectively than benidipine. However, the combination of ATP + benidipine further reduced bevacizumab-induced renal toxicity relative to benidipine or ATP alone. These data indicate that ATP + benidipine might be a potential therapeutic strategy for the prevention of bevacizumab-induced renal toxicity.

Protective effect of lutein against acrolein-induced ototoxicity in rats.

BACKGROUND: Acrolein is a reactive aldehyde that forms during burning of wood and other fuels. It is also a product of lipid peroxidation (LPO) reactions and is present in cigarette smoke. Acrolein is known to cause oxidative stress and inflammatory nerve tissue damage. Lutein is a tetraterpenoid molecule with antioxidant and anti-inflammatory properties. There appear to be no studies on the effect of lutein on vestibulocochlear nerve damage induced by acrolein. The aim of this study was to investigate the effect of lutein on vestibulocochlear nerve damage induced by acrolein in rats using biochemical and histopathological methods. METHODS: The rats were divided into three groups (n = 6, for each group) a healthy control group (HG), an acrolein (ACR) group and a lutein and acrolein (LACR) group. In the LACR group, lutein was administered (1 mg/kg) via oral gavage. The ACR and HG groups received saline via oral gavage. Then, 1 h after the administration of lutein and saline, the LACR and ACR groups were treated with 3 mg/kg of acrolein via oral gavage. This procedure was repeated once a day for 30 days. RESULTS: The results of biochemical experiments showed that in the vestibulocochlear nerve tissues of the animals treated with acrolein, the levels of malondialdehyde, total oxidants, nuclear factor kappa b, tumor necrosis factor alpha and interleukin 1 beta significantly increased, whereas the levels of total glutathione and total antioxidants decreased as compared to those in the HG and LACR groups. In addition, severe histopathological damage was observed in vestibulocochlear nerve tissue of the acrolein group, whereas this damage was alleviated in the lutein group. CONCLUSION: Lutein protected vestibulocochlear nerve tissue from acrolein-associated oxidative and proinflammatory damage. This suggests that lutein might be useful in preventing or treating acrolein-induced ototoxicity.

The effect of adenosine triphosphate on propofol-induced myopathy in rats: a biochemical and histopathological evaluation.

Propofol infusion syndrome characterized by rhabdomyolysis, metabolic acidosis, kidney, and heart failure has been reported in long-term propofol use for sedation. It has been reported that intracellular adenosine triphosphate (ATP) is reduced in rhabdomyolysis. The study aims to investigate the protective effect of ATP against possible skeletal muscle damage of propofol in albino Wistar male rats biochemically and histopathologically. PA-50 (n = 6) and PA-100 (n = 6) groups of animals was injected intraperitoneally to 4 mg/kg ATP. An equal volume (0.5 ml) of distilled water was administered intraperitoneally to the P-50, P-100, and HG groups. One hour after the administration of ATP and distilled water, 50 mg/kg propofol was injected intraperitoneally to the P-50 and PA-50 groups. This procedure was repeated once a day for 30 days. The dose of 100 mg/kg propofol was injected intraperitoneally to the P-100 and PA-100 groups. This procedure was performed three times with an interval of 1 days. Our experimental results showed that propofol increased serum CK, CK-MB, creatinine, BUN, TP I, ALT, AST levels, and muscle tissue MDA levels at 100 mg/kg compared to 50 mg/kg and decreased tGSH levels. At a dose of 100 mg/ kg, propofol caused more severe histopathological damage compared to 50 mg/ kg. It was found that ATP prevented propofol-induced muscle damage and organ dysfunction at a dose of 50 mg/kg at a higher level compared to 100 mg/kg. ATP may be useful in the treatment of propofol-induced rhabdomyolysis and multiple organ damage.

How do routine laboratory tests change in coronavirus disease 2019?

How the routine laboratory tests change in terms of coronavirus disease 2019 (COVID-19) was retrospectively analyzed in a large group of patients. Biochemical, hematological and inflammatory variables of a totaly 555 (n = 532 in non-intensive care unit (non-ICU), n = 23 in ICU) patients diagnosed with COVID-19 were analyzed accessing them through the laboratory information system. White blood cell (WBC), neutrophil (NEU), platelet large cell ratio, neutrophil to lymphocyte ratio (NLR), derived NLR (d-NLR), aspartate aminotransferase, urea, creatine kinase (CK) myocardial band (CK-MB), procalcitonin (PCT) values were high whereas lymphocyte (LYM), eosinophil, red blood cells (RBC), hemoglobin, lymphocyte to monocyte ratio, estimated glomerular filtration rate values were low in the ICU group when compared with non-ICU. WBC, NEU, red cell distribution width, alanine transaminase, creatinine, urea, CK-MB, CK, direct bilirubin, lactate dehydrogenase, glucose, C-reactive protein, erythrocyte sedimentation rate, ferritin, D-dimer, PCT and international normalized ratio values increased while RBC, hemoglobin, hematocrit, mean corpuscular volume and total bilirubin values decreased in a significant proportion of patients in both groups based on the normal reference ranges. LYM count was found to be low in a significant number of patients (57.5%) especially in the ICU group and as an important risk factor and diagnostic parameter on admission to ICU (OR: 125, AUC: 0.74). Routine laboratory tests provide important information in terms of both diagnosis and severity of COVID-19. Lymphopenia is a condition that should be monitored which indicates the severity of the disease.

Effects of pycnogenol on ischemia/reperfusion-induced inflammatory and oxidative brain injury in rats.

BACKGROUND: Ischemia/reperfusion (I/R) injury results from the onset of re-circulation following a perfusion deterioration period in the tissues, resulting in more damage than that caused by perfusion deterioration. This study aimed to determine the effects of pycnogenol on I/R injury in rat brain tissues. METHODS: Eighteen albino Wistar rats were divided into three groups: I/R injury (IR, n = 6) group; I/R injury + pycnogenol (IR + P, n = 6) group; and sham group (SG, n = 6). After 30 min of transient ischemia, 24 h of reperfusion was achieved in the IR and IR + P groups. Surgical dissection, except for transient ischemia, was performed in SG. Next, histopathological and biochemical investigations were performed on brain tissues. Malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPO) were analyzed as oxidative stress markers; IL-1ß and TNF-α were analyzed as inflammatory stress markers in biochemical tests. RESULTS: Histopathological examination revealed normal morphology in SG and diffuse cortex damage with edema, vasopathology, and inflammatory cell infiltration in the IR group. The IR + P group showed less cortex damage, edema, and vasopathology than the IR group. The MDA, IL-1ß, and TNF-α levels were significantly higher in the IR group than those in the SG group. The values of same markers for the IR + P group were significantly lower than the IR group. The GSH and GPO levels were significantly decreased with IR damage, but PYC treatment showed significant improvement in the levels. CONCLUSION: This study showed that the administration of pycnogenol ameliorated brain damage after I/R injury by reducing oxidative and inflammatory damage in the rat brain.

Does myo-inositol oxygenase, the only enzyme to catalyze myo-inositol in vivo, play a role in the etiology of polycystic ovarian syndrome?

In polycystic ovary syndrome (PCOS), myo-inositol (MI) supplements have shown many beneficial effects. In this study, therefore, we aimed to investigate the serum level of myo-inositol oxygenase (MIOX), which is the only enzyme catalyzing MI in vivo, in patients with PCOS. Serum MIOX enzyme levels and other laboratory parameters were compared between sixty patients, who were diagnosed with PCOS for the first time, and sixty healthy individuals at similar age and sex. MIOX serum levels were not different between two groups (p = 0.7428). MIOX median and 95% CI were 19.4 and 10.6-39.1 in the control group and 16.4 and 7.6-46.2 in the patient group respectively. Demographic data, biochemical and hematological parameters, hormone parameters were not different except from the lymphocyte count between the two groups. Lymphocyte count was higher in the patient group. Although the ratio of LH/FSH was higher in the patient group, it was not statistically significant. Our results suggest that serum MIOX levels do not change in PCOS. It was, therefore, concluded that MI deficiency observed in PCOS was not related to the level of MIOX enzyme which cleaves MI.

Effects of nimesulide on the small intestine mucositis induced by methotrexate in rats.

Intestinal mucositis is one of the major problems in the patients receiving cancer treatment. Nimesulide is a drug with antioxidant, antiinflammatory and antiulcer features. We aimed to investigate the effect of nimesulide on the small intestine mucositis induced by methotrexate (MTX) in rats. Experimental animals were divided into the control group, MTX group (MTXG) and nimesulide+MTX administered group (NMTXG) with eight rats per group. The control and MTXG groups were given distilled water by gavage and the NMTXG was given nimesulide 100 mg/kg orally. After one hour, the NMTXG and MTXG rat groups were administered oral MTX 5 mg/kg. This procedure was repeated once a day for 15 days and the rats were sacrificed. The duodenum and jejunum of each rat was removed for the assessment of biochemical markers and histopathological evaluation. Malondialdehyde (MDA) and myeloperoxidase (MPO) levels were significantly higher in the duodenal and jejunal tissues of the animals which received MTX, compared to the control and NMTXG (P<0.001). Also, the levels of total glutathione (tGSH), glutathione reductase (GSHRd), glutathione peroxidase (GSHPx), catalase (CAT) and superoxide dismutase (SOD) were significantly lower in the MTXG (P<0.001) compared to other groups. MTX led to villus and crypt epithelial damage and inflammation containing marked PMNL and eosinophils in the intestinal tissues histopathologically. Whereas, there was only mild irregularities in the villus structures of the NMTXG. Nimesulide protected the small intestines against damage by MTX. Intestinal mucositis caused by MTX may be preventable by co-administered nimesulide.

Can thiamine pyrophosphate prevent desflurane induced hepatotoxicity in rats?

PURPOSE: To investigate the effects of thiamine pyrophosphate (TPP) against desflurane induced hepatotoxicity. METHODS: Thirty experimental animals were divided into groups as healthy (HG), desflurane control (DCG) , TPP and desflurane group (TDG). 20 mg/kg TPP was injected to intraperitoneally TDG. After one hour of TPP administration, desflurane was applied for two hours. After 24 hours, liver tissues of the animals killed with decapitation were removed. The oxidant/antioxidant levels and ALT, AST and LDH activities were measured. The histopathological examinations were performed in the liver tissues for all rats. RESULTS: Notwithstanding the levels of oxidants and liver enzymes were significantly increased (p<0.0001), antioxidant levels were significantly decreased in DCG (p<0.0001). On contrary to the antioxidant parameters were increased (p<0.05) the oxidant parameters and liver enzymes were decreased in TDG (p<0.0001). Whereas multiple prominent, congestion, hemorrhage and dilatation were observed in sinusoids and lymphocyte-rich inflammation results in the centrilobular and portal areas of liver tissue in DCG, these findings were observed less frequently in TDG. CONCLUSION : Thiamine pyrophosphate prevented liver oxidative damage induced with desflurane and may be useful in prophylaxis of desflurane induced hepatotoxicity.