Acacetin ameliorates acetylsalicylic acid-induced gastric ulcer in rats by interfering with oxidative stress, inflammation, and apoptosis

Gastric ulcer (GU) is a benign lesion in which excessive acid and pepsin activity affects the mucosal ep- ithelium and is common worldwide. Gastrointestinal disturbances come to the fore among the side effects observed in the treatment with drugs such as aspirin. Acacetin is a plant-derived flavonoid with intriguing properties such as anti-inflammatory, antioxidant, and anticancer. The aim of the study is to investigate the effects of acacetin in GU model caused by aspirin active ingredient acetylsalicylic acid. Methods: Thirty-two Wistar albino rats were divided into four groups: Control, GU, acacetin, and GU +acacetin. Acetyl- salicylic acid (150 mg/kg) and acacetin (25 mg/kg) were administered intraperitoneally as a single dose. Gastric lesions were examined microscopically and macroscopically. TNF-a, cyclooxygenase-2 (COX-2), and nuclear factor kappa B (NF-kB) for inflammation; Caspase-3 and Bcl-2 for apoptosis, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) for oxidative stress were analyzed. Results: Bcl-2 and TAS values were decreased, while Tumor necrosis factor-alpha (TNF-α), COX-2, NF-kB, Caspase-3, TOS, and OSI values were increased in the GU group compared to the control group. Bcl-2 and TAS values were increased and TNF-α, COX-2, NF-kB, Caspase-3, TOS, and OSI values were decreased in the GU +acacetin group compared to the GU group. The GU index (GUI) detected in the GU group decreased significantly with the administration of acacetin. Conclusion: High doses of ASA contributed to the formation of GU in the stomach tissue by increasing the levels of inflammation, oxidative stress, and apoptosis, whereas ACA reduced the ulcer damage by reducing the increase in all these pathways

A histological and biochemical study of the protective role of hesperidin in testicular ischemia-reperfusion injury

This study aimed to investigate the possible effects of hesperidin on ischemia-reperfusion (IR) injury applied to rat testis. Methods: Twenty-eight Wistar albino rats were used and divided into four groups of seven each. Group 1: Sham surgery was performed on the right testis. Group 2: Hesperidin 100 mg/kg was administered intraperitoneally to rats. Group 3: After 1 h of ischemia and 4 h of reperfusion, the testicles were removed. Group 4: 100 mg/kg hesperidin was given 30 min before reperfusion. Biochemical, immunohistochemical, and histopathological analyzes were performed on testicles obtained from each group. Results: Total oxidant status (TOS) and oxidative stress index (OSI) levels increased significantly in the IR and IR-He groups (respectively, p=0.016, p=0.041; p=0.01, and p=0.024). TOS and OSI values in the hesperidin group decreased, although not statistically significant, compared to the IR group. Tumor necrosis factor-alpha (TNF-α) and nuclear factor kappa B (NF-kB) values were decreased in the hesperidin group compared to the IR group, although it was not statistically significant. Caspase-3 levels in testicular tissue were significantly increased in the IR group compared to the hesperidin group (p<0.05). While there were degenerative changes in the testicular tissue in the IR groups, a decrease in bleeding, congestion, edema, and degenerative changes was observed in the hesperidin-administered groups. Conclusion: Hesperidin reduced oxidative stress (decreased total oxidant level and OSI), inflammation (TNF-α), and apoptosis (NF-kB and caspase-3). According to these results, it was observed that hesperidin application had a protective effect on IR injury

Protective effect of astaxanthin and metformin in the liver of rats in which the polycystic ovary syndrome model was formed by giving letrozole

Objective(s): In this study, the effects of astaxanthin on liver tissue in rats with polycystic ovary syndrome (PCOS) were evaluated.Materials and Methods: Fifty-four Spraque-Dawley rats were divided into 9 groups: Groups: Control, PCOS, PCOS+Metformin (Met), PCOS+ Astaxanthin (ASX)10, PCOS+ASX20, PCOS+ASX40, PCOS+Met+ASX10, PCOS+Met+ASX20, and PCOS+Met+ASX40. PCOS was induced in female rats by oral administration of letrozole (1 mg/kg) for 21 days. Rats were treated with ASX (10 mg/kg), ASX (20 mg/kg), ASX (40 mg/kg), and metformin (20 mg/kg) for 7 days after PCOS induction. At the end of the experiment, malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured in the liver tissue. The liver was stained with hematoxylin/eosin for histological examination. Additionally, NF-kB and caspase 3 were analyzed immunohistochemically.Results: A remarkable abnormality was observed in the biochemical and histological parameters in the liver tissue of the PCOS model rats. Astaxanthin dose-dependently normalized the MDA level. Additionally, astaxanthin showed a protective effect by increasing the SOD level and increasing its antioxidant activities. We observed that administration of astaxanthin in addition to metformin applied in the standard was more effective. Caspase 3 and NF-kB immune positivity was lower in the groups given astaxanthin compared with PCOS. Histologically, it was observed that astaxanthin improved the deteriorated liver morphology in the letrozole-induced PCOS group.Conclusion: According to our results, it was observed that astaxanthin had antioxidant, anti-inflammatory and anti-apoptotic effects on PCOS in the treatment groups. Therefore, it was concluded that astaxanthin may have a protective effect against PCOS side effects

Hepatoprotective effects of B-1,3-(D)-Glucan on bortezomib-induced liver damage in rats

The aim of this study was to evaluate the effects of beta -1,3-(D)-glucan as an antioxidant and tissue protective agent and study the biochemical, histopathologic, and immunohistochemical effects of first therapeutic proteasome inhibitor bortezomib on the liver for treating relapsed multiple myeloma. The experiment included 36 adult male rats, which were divided into four treatment groups: control (healthy); bortezomib-treated; beta-1,3-D-glucan-treated; and bortezomib + beta-1,3-(D)-glucan-treated. Each group was subdivided into two subgroups based on time of sacrifice (48 or 72 h). After the experiments, superoxide dismutase (SOD) activity and lipid peroxidation (LPO) amounts were determined, and immunohistochemical and histopathological changes were examined in all rat liver tissues. beta -1,3-(D)-Glucan treatment normalized changes of LPO and stimulated an over activity of endogenous SOD. The results of the histopathologic parameters showed that treatment with beta -1,3-(D)-Glucan in the bortezomib group ameliorated the development of non-specific reactive hepatitis (NSRH) and Kupffer cell activation via NF-kB. Administration of beta -1,3-(D)-Glucan is effective in reversing tissue damage induced by bortezomib in rat livers.Bu çalışmanın amacı, relaps multiple miyelom tedavi etmek için kullanılan ilk terapötik proteazom inhibitörü olan bortezomibin karaciğer üzerine immunohistokimyasal, histopatolojik ve biyokimyasal etkilerini araştırmak ve bir antioksidant ve doku koruyucu ajan olarak B-1,3-(D)-glukanın etkilerini değerlendirmekdi. Deney; kontrol (sağlıklı), bortezomib ile tedavi, B-1,3-(D)-glukan ile tedavi ve bortezomib + B-1,3-(D)-glukan ile tedavi olmak üzere dört tedavi grubuna bölünen 36 yetişkin erkek sıçan içerdi. Her bir grup sakrifikasyon zamanına (48 veya 72 saat) göre iki alt gruba ayrıldı. Deneylerin bitiminden sonra, süperoksit dismutaz (SOD) aktivitesi ve lipid peroksidasyon (LPO) miktarları ölçüldü ve tüm sıçan karaciğer dokularında immünohistokimyasal ve histopatolojik değişiklikler incelendi. B-1,3-(D)-glukan ile tedavi LPO değişikliğini normalize etti ve endojen SOD aktivitesi aşırı uyardı. Histopatolojik parametrelerin sonuçları, bortezomib grubunda B-1,3-(D)-glukan ile tedavi NF-kB yoluyla Kupffer hücre aktivasyonunu ve non-spesifik reaktif hepatit (NSRH) gelişimini regüle ettiğini gösterdi. B-1,3-(D)-glukan uygulaması, sıçan karaciğerinde bortezomibin neden olduğu geri döndürülebilir doku hasarında efektifdir

The effect of platelet-rich plasma injection on post-internal urethrotomy stricture recurrence

[No abstract available

Carvacrol reduces abnormal and dead sperm counts by attenuating sodium arsenite-induced oxidative stress, inflammation, apoptosis, and autophagy in the testicular tissues of rats

Arsenic (As) is a highly toxic metalloid. Carvacrol (CAR) is the active ingredient of Lamiaceae plants and has various biological and pharmacological properties. The present study investigated the protective effects of carvacrol (CAR) against testicular toxicity induced by sodium arsenite (SA). Rats were given SA (10 mg/kg) and/or CAR (25 or 50 mg/kg) for 14 days. Semen analyzes showed that CAR increased sperm motility and decreased the percentage of abnormal and dead sperm. It was determined that the oxidative stress induced by SA decreased with the increase of Nrf-2 and HO-1 expressions, SOD, CAT, GPx, and GSH levels, and MDA levels decreased after CAR treatment. It was observed that autophagy and inflammation triggered by SA in testicular tissue were alleviated by suppressing the expressions of LC3A, LC3B, MAPK-14, NF-κB, TNF-α, IL-1β, iNOS, and COX-2 biomarkers in rats given CAR. Also, CAR treatment suppressed SA-induced apoptosis by inhibiting Bax and Caspase-3 expressions in testicles and up-regulating Bcl-2 expression. Histopathological analyzes showed that rats given SA had deterioration in tubule structure and spermatogenesis cell line, especially a serious loss of spermatogonia cells, atrophy of seminiferous tubules, and deterioration of germinal epithelium. In the group given CAR, the germinal epithelium and connective tissue were in normal morphological structure and an increase in seminiferous tubule diameters was observed. As a result, it was determined that oxidative stress, inflammation, autophagy, and apoptosis induced by SA were suppressed by CAR, thus protecting the testicular tissue from damage and increasing semen quality

Zingerone reduces sodium arsenite-induced nephrotoxicity by regulating oxidative stress, inflammation, apoptosis and histopathological changes

Arsenic is widely available in the environment and arsenic toxicity is a public health problem of serious concern worldwide. Zingerone is a promising phytochemical with various pharmacological effects. In this study, the potential protective effect of zingerone against sodium arsenite (NaAsO2, SA) induced nephrotoxicity was investigated. Thirty-five male Sprague-Dawley rats were divided into five different groups as control, zingerone, SA, SA + zingerone 25, SA + zingerone 50. SA was administered alone at a dose of 10 mg/kg for 14 days or given 30 min before zingerone (25 mg/kg or 50 mg/kg) treatment. At the end of the experiment, the kidney tissues was examined biochemically, molecularly and microscopically. SA toxicity was associated with increased malondialdehyde level, whereas glutathione, superoxide dismutase, catalase, and glutathione peroxidase were decreased. Administration of SA caused inflammation in the kidney tissue by upregulation of NF-κB and IL-1β, TNF-α, IL-6, iNOS, COX-2, MAPK14, MAPK15, JNK. SA administration caused apoptosis in the kidney by upregulating caspase-3 and Bax levels and downregulating Bcl-2, and autophagy by activating beclin-1. Also, SA administration showed a suppressive effect on AKT2 and FOXO1 mRNA transcript levels. All these factors impair kidney function and increase creatinine and urea levels, resulting in pathological changes and a decrease in nephrin. Treatment with zingerone at doses of 25 and 50 mg/kg significantly reduced oxidative stress, inflammation, apoptosis and autophagy in kidney tissue. In addition, it was confirmed by histological evaluation as well as serum urea and creatinine levels that kidney damage due to SA toxicity can be modulated by zingerone administration

Protective effects of sinapic acid against lead acetate-induced nephrotoxicity: a multi-biomarker approach

Lead acetate (PbAc) is one of the top five most dangerous toxic heavy metals, particularly leading to kidney damage and posing serious health risks in both humans and animals. Sinapic acid (SNP) is a naturally occurring flavonoid found in fruits and vegetables that stands out with its antioxidant, anti-inflammatory, and anticancer properties. This is the first study to investigate the effects of SNP on oxidative stress, inflammation, apoptosis, autophagy and endoplasmic reticulum (ER) stress in PbAc-induced nephrotoxicity in rats by biochemical, molecular and histological methods. 35 Spraque dawley rats were randomly divided into five groups of 7 rats each: control, PbAc, SNP (10mg/kg), PbAc + SNP 5, PbAC + SNP 10. PbAc at a dose of 30 mg/kg body weight was administered via oral gavage alone or in combination with SNP (5 and 10 mg/kg body weight) via oral gavage for seven days. While PbAc impaired renal function by increasing serum urea and creatinine levels, SNP decreased these levels and contributed to the improvement in renal function. The administration of SNP reduced oxidative stress by increasing PbAc-induced decreased antioxidant enzyme (SOD, CAT, and GPx) activities and GSH levels, decreasing MDA levels, a marker of increased lipid peroxidation. SNP administration reduced NF-κB, TNF-α, IL-1β, NLRP3, and RAGE mRNA transcription levels, NF-κB, and TNF-α protein levels that are among the PbAc-induced increased inflammation parameters. Decreases in antiapoptotic Bcl-2 and increases in apoptotic Bax, APAF-1, and Caspase-3 due to PbAc exposure, SNP reversed the situation. SNP reduced ER stress caused by PbAc by increasing PERK, IRE1, ATF-6, CHOP, and GRP-78 levels and made it tend to regress. SNP reduced autophagy damage by decreasing the Beclin-1 protein level increased by PbAc. The findings of the present study suggested that SNP attenuates PbAc-induced nephrotoxicity

Gossypin protects against renal Ischemia-Reperfusion Injury in rats

*Akaras, Nurhan ( Aksaray, Yazar )Renal injury occurring as a result of renal ischemia-reperfusion may lead to renal failure or even death. The aim of this study is to investigate possible protective effects of Gossypin on tissue damage occurred due to ischemia-reperfusion in rat kidney tissue. A total of 48 male Wistar albino rats were used in the study. These rats were randomly divided into 6 groups equally (n = 8). The created groups were control (C), sham (S), ischemia-reperfusion (I/R), I/R + DMSO, I/R + 400 mu g/kg gossypin and I/R + 4 mg/kg gossypin. In the rats of sham group, the right nephrectomy was performed. In the rats of other groups rather than sham, the left renal artery was clamped after performing the right nephrectomy. Gossypin was administered intraperitoneally before the reperfusion. 24 h reperfusion was applied to the left renal after 1 h of ischemia. TNF-alpha, IL-1 beta, IL-6 and IL-10 levels were measured with spectrophotometric methods in the kidney tissues after the procedures were completed. Apoptosis and inflammatory pathways were evaluated histopathologically using Caspase 3 and NF-kappa B antibodies. There was a statistically significant decrease in IL-1 beta and IL-6 levels of the gossypin groups compared to the I/R group (P<0.05). As the level of TNF-alpha was decreased in the gossypin administered groups compared to the I/R group although not statistically significant, the level of IL-10 was increased. In the present study, we aimed to show that gossypin in renal I/R model is effective on inflammatory process and apoptosis and that it can be used in routine treatment to decrease the damage in all reasons that may cause I/R. In addition, this study can shed light on the studies to be done in this field in the future...

Beneficial effects of Chrysin on Cadmium-induced nephrotoxicity in rats: Modulating the levels of Nrf2/HO-1, RAGE/NLRP3, and Caspase-3/Bax/Bcl-2 signaling pathways

Cadmium (Cd) is a toxic heavy metal that targets the kidney directly in the body. Chrysin (CHR) is a natural flavonoid with many properties such as antioxidant, anti-inflammatory and anti-apoptotic. The current study discloses new evidence as regards of the curative effects of CHR on Cd-induced nephrotoxicity by regulating oxidative stress, apoptosis, autophagy, and inflammation. Cd was administered orally at a dose of 25 mg/kg body weight alone or in combination with orally administered CHR (25 and 50 mg/kg body weight) for 7 days. Biochemical, molecular, and histological methods were used to investigate inflammation, apoptosis, autophagy, and oxidant pathways in renal tissue. Renal function tests were also evaluated. Cd caused an increase in serum toxicity markers, lipid peroxidation and a decrease in the activities of antioxidant enzymes. Nrf-2 triggered inflammatory responses by suppressing HO-1 and NQO1 mRNA transcripts and increasing NF-κB, TNF-α, IL-1β and iNOS mRNA transcripts. Cd caused inflammasome by increasing RAGE and NLRP3 mRNA transcripts. In addition, Cd application caused apoptosis by increasing Bax, Apaf-1 and Caspase-3 mRNA transcripts and decreasing Bcl-2 mRNA transcript level. It caused autophagy by increasing the activity of Beclin-1 level. CHR treatment had the opposite effect on all these values and reduced the damage caused by all these signal pathways. Overall, the data of this study indicate that renal damage associated with Cd toxicity could be ameliorated by CHR administration