Analgesic effect of erector spinae plane block after cesarean section: A randomized controlled trial.

Background: Ultrasound-guided bilateral erector spinae plane block is also a technique for providing analgesia after a cesarean section. Aim: We hypothesized that bilateral erector spinae plane block applied from the transverse process of T9 who underwent elective cesarean section could provide effective postoperative analgesia. Patients and Methods: Fifty parturients who were scheduled to undergo elective cesarean section under spinal anesthesia were included in the study. Group SA (n = 25) was categorized as the group in which spinal anesthesia alone (SA) was performed, and Group SA+ESP (n = 25) was categorized as the group in which SA + ESP block was performed. All patients were given a solution containing 7 mg isobaric bupivacaine + 15 µg fentanyl intrathecally through spinal anesthesia. In the SA + ESP group, the bilateral ESPB was performed at level T9 with 20 ml 0.25% bupivacaine + 2 mg dexamethasone immediately after the operation. Total fentanyl consumption in 24 h, the visual analogue scale for pain, and time to the first analgesic request were evaluated postoperatively. Results: The total fentanyl consumption in 24 h was statistically significantly lower in the SA + ESP group than the SA group (279 ± 242.99 µg vs. 423.08 ± 212.55 µg, respectively, P = 0.003). The first analgesic requirement time was statistically significantly shorter in the SA group than the SA + ESP group (150.20 ± 51.83 min vs. 197.60 ± 84.49 min, respectively, P = 0.022). Postoperative VAS scores at 4th, 8th, and 12th h at rest were statistically significantly lower in group SA + ESP than in group SA (P = 0.004, P = 0.046, P = 0.044, respectively). VAS scores during the postoperative 4th, 8th, and 12th h cough were statistically significantly lower in group SA + ESP than in group SA (P = 0.002, P = 0.008, P = 0.028, respectively). Conclusion: Ultrasound-guided bilateral ESP provided adequate postoperative analgesia and significantly decreased postoperative fentanyl consumption in patients having cesarean section. Also, it has a longer analgesia time than the control group, and it has been shown to delay the first analgesic requirement.

Agomelatine protects heart and aorta against lipopolysaccharide-induced cardiovascular toxicity via inhibition of NF-kß phosphorylation.

The aim of this study was to investigate the possible ameliorating effects of agomelatine (AGO) on lipopolysaccharide (LPS)-induced endothelial and cardiac damage. Twenty-four female Wistar Albino rats divided into 3 groups as follows: Control, LPS and LPS + AGO. Total oxidant status (TOS), total antioxidant status (TAS), nuclear factor kappa beta (NF-kß)/p65, p-NF-kß, full caspase-8 (Cas-8) and cleaved cas-8 levels were measured in cardiac tissues and creatine kinase MB (CKMB), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) levels in blood biochemically. In addition; cas-8, sirtuin-1 (SIRT-1), interleukin-4 (IL-4), interleukin-10 (IL-10), haptoglobin measured histopathologically in cardiac and aortic tissues. The levels of CKMB, AST, LDH and TOS were increased and TAS were decreased in the LPS group. In Western blot analyses NF-kß/p65, p-NF-kß/p65, full and cleaved cas-8 protein levels increased in cardiac tissues of LPS group. In histopathological and immunohistochemical evaluation of the heart sections; hyperemia, micro-hemorrhages and inflammatory cell infiltrations, increase of cas-8, haptoglobin, IL-4 and IL-10 and decrease of SIRT-1 levels were observed in cardiac and endothelial tissues of LPS groups. AGO treatment reversed all these parameters. It was shown that LPS-induced inflammation, oxidative stress and apoptosis via increasing of NF-kß/p65 signaling, decreasing of SIRT-1 levels and increase of cas-8 levels in heart and endothelial tissues respectively. AGO corrected all these parameters by its antioxidant, antiinflammatory and antiapoptotic activities.

Agomelatine could prevent brain and cerebellum injury against LPS-induced neuroinflammation in rats.

Sepsis, systemic hyper-inflammatory immune response, causes the increase of morbidity and mortality rates due to multi-organ diseases such as neurotoxicity. Lipopolysaccharide (LPS) induces inflammation, oxidative stress and apoptosis to cause brain damage. We aimed to evaluate the antioxidant, anti-inflammatory and antiapoptotic effects of Agomelatine (AGM) on LPS induced brain damage via NF-kB signaling. Twenty-four animals were divided into three groups as control, LPS (5 mg/kg) and LPS + AGM (20 mg/kg). Six hours after the all administrations, rats were sacrificed, brain tissues were collected for biochemical, histopathological and immunohistochemical analysis. In LPS group; total oxidant status (TOS), OSI index, Caspase-8 (Cas-8), NF-kß levels increased and Total antioxidant status (TAS) levels decreased biochemically and Cas-8, haptoglobin and IL-10 expressions increased and sirtuin-1 (SIRT-1) levels decreased immunohistochemically. AGM treatment reversed these parameters except haptoglobin levels in hippocampus and SIRT-1 levels in cerebellum. Besides, AGM treatment blocked the phosphorylation of NF-kB biochemically and ameliorated increased the levels of hyperemia, edema and degenerative changes histopathologically. In conclusion, AGM enhanced SIRT-1 levels to negatively regulate the transcription and activation of p-NF-kB/p65 which caused to ameliorate inflammation, oxidative stress and apoptosis.

Anti-inflammatory and antiresorptive functions of melatonin on experimentally induced periapical lesions.

AIM: To investigate the effects of systemically administered melatonin on inflammation and alveolar bone resorption in rats with experimentally induced periapical lesions. METHODOLOGY: Thirty adult Sprague Dawley rats were divided equally into negative, positive control and melatonin groups. The pulp chambers of their mandibular first molars were exposed to the oral environment to induce experimental periapical lesions in the positive control and melatonin groups. The melatonin group received daily intraperitoneal injections of melatonin at a dose of 10 mg kg-1 . After 21 days, the animals were euthanized; the hemi-mandible parts were prepared for radiological, histopathological, immunohistochemical (IL-1ß, RANK, RANKL, OPG and tartrate-resistant acid phosphatase (TRAP) and Brown-Brenn (bacteria) evaluations. Data were analysed by Kruskal-Wallis (for non-parametric data) and one-way anova tests (for parametric data) (P < 0.05). RESULTS: The area of radiographic periapical bone loss was significantly smaller in rats that were given daily intraperitoneal injections of melatonin (P < 0.01). The histopathological scores of the melatonin group were significantly lower than those of positive control group (P < 0.01). Histomorphometrically, the area of periapical bone loss in the melatonin group was significantly smaller than the positive control group (P < 0.01). The expression of IL1-ß, RANK and RANKL was significantly higher in the positive control group, whereas OPG was significantly higher in the melatonin group (P < 0.01). The number of osteoclasts was significantly greater in the positive control group by TRAP staining analyses (P < 0.01). The scores for bacteria localization using Brown-Brenn staining in the melatonin group was significantly lower than that of the positive control group (P < 0.01). CONCLUSIONS: Melatonin demonstrated antiresorptive effects on bone associated with experimentally induced periapical lesions in rats via its anti-inflammatory activity. Further studies are necessary to evaluate its possible effects on the healing of periapical lesions.

Comparison of efficiency of hyaluronic acid and/or bone grafts in healing of bone defects.

BACKGROUND: Reconstruction of bone defects in oral and maxillofacial surgery has widespread uses. In recent years, the capacity of various biomaterials alone or in combination with bone graft materials to increase bone healing has been an intensive research topic. The aim of this study is to evaluate the efficacy of hyaluronic acid and/or bone graft material on bone healing in defects created in the rat mandible. Methods: In our study, rats were divided into 4 groups. Group 1 is designated to be treated with no materials, Group 2 with graft material, Group 3 with only hyaluronic acid, and Group with hyaluronic acid and graft material. A critical-size defect of 5 mm in diameter was created bilaterally in the rat mandibles and the rats were divided into the indicated groups accordingly. At the end of the postoperative 6th week, the experiment was terminated. The right halves of the mandibles were evaluated immunohistochemically and histopathologically in terms of bone healing, and the left in terms of mineralization level via microcomputed tomography. RESULTS: Histopathological evaluation showed that healing in the empty group was significantly lower than the other groups that were treated with materials (P < 0.05); but the difference between the material-treated groups was not significant. Immunohistochemical evaluation revealed that the staining was moderately positive/strongly positive in all groups, but the difference between the groups was not significant. The highest mineralization values observed in the defected areas that belonged to 2 groups using hyaluronic acid, and the difference between them was found to be statistically significant (P < 0.05). The lowest mineralization values observed in the defected areas was most frequent in the group where only the hyaluronic acid was used, and there was a statistically significant difference between the other groups (P < 0.05). CONCLUSION: In conclusion, the use of hyaluronic acid alone or in combination with bone grafting has been shown to contribute positively to the improvement of bone defects in the jaw area.

Effects of rosuvastatin on inducible nitric oxide synthase in rats with hyperlipidaemia and periodontitis.

BACKGROUND AND OBJECTIVE: Nitric oxide is a free radical that is synthesized from l-arginine by nitric oxide synthase (NOS). The level of inducible NOS (iNOS) in gingiva with periodontitis is higher than that in healthy gingiva. The aim of this study was to evaluate the effects of rosuvastatin administration on alveolar bone loss (ABL) and iNOS(+) cell counts in gingival tissues in rats with ligature-induced experimental periodontitis with/without hyperlipidaemia. MATERIAL AND METHODS: The rats were randomly divided into seven groups: Hy (cholesterol-added diet/water administration); HyP (cholesterol-added diet/periodontitis/water administration); HyPR (cholesterol-added diet/periodontitis/rosuvastatin administration); P (standard diet/periodontitis/water administration); PR (standard diet/periodontitis/rosuvastatin administration); C (standard diet/water administration); and R (standard diet/rosuvastatin administration). Experimental periodontitis was induced with silk ligatures, and rosuvastatin/water was administered to rats by oral gavage for the last 2 weeks of the 8-week study. After the rats were killed in week 8, histomorphometric and histological analyses were performed. Immunostained iNOS(+) cells were counted in the gingival samples and the Mann-Whitney U-test was used for statistical analysis. RESULTS: The experimental groups exhibited increases in total cholesterol and low-density lipoprotein, except for Groups C and R. The cholesterol-added diet induced ABL in Group Hy. Of the periodontitis groups, the lowest ABL was found in Group PR. While there was a significant difference in ABL between Groups P (0.82 ± 0.15 mm) and PR (0.70 ± 0.21 mm) receiving a standard diet (P < .05), no difference was observed between Groups HyP (0.77 ± 0.07 mm) and HyPR (0.76 ± 0.11 mm) receiving a cholesterol-added diet (P Ëƒ .05). Rosuvastatin significantly reduced expression of iNOS in Groups PR (18.40 ± 2.31%) and HyPR (24.00 ± 4.83%) compared with Group P (30.90 ± 2.42%; P < .001). However, a larger number of iNOS(+) cells was found in Group HyPR than in Group PR (P < .001). CONCLUSION: Administration of rosuvastatin reduced gingival iNOS expression in ligature-induced periodontitis with/without hyperlipidaemia. It also led to significant differences in ABL in rats with periodontitis, except when periodontitis was associated with hyperlipidaemia. These findings could provide an important contribution in further studies to evaluate the role of rosuvastatin as a host modulatory agent in the pathogenesis of periodontal diseases.

Correlation between clinical findings and eosinophil/neutrophil ratio in patients with nasal polyps.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a frequent disease which can be classified as eosinophilic or neutrophilic based on dominant inflammatory cell type at tissue. The aim of this study was to evaluate the clinical relevance of classifying nasal polyps as eosinophilic or neutrophilic on treatment outcomes. The study was conducted with 40 patients who underwent either surgical or medical treatment with the diagnosis of CRSwNP. The patients were classified into two groups for further assessment up to eosinophil intensity at polyp tissue. All patients were examined by nasal endoscopy and paranasal computed tomography (CT). Before treatment, subjective symptom score, nasal endoscopy score, and CT score were measured. Subsequently, they were reevaluated by similar diagnostic tests after either medical or surgical treatment at sixth month. The preoperative subjective symptom score, endoscopy score, and paranasal CT score were compared between chronic rhinosinusitis (CRS) with eosinophilic nasal polyps (E-NP) (CRSwE-NP) group and CRS with neutrophilic nasal polyps group and there was no difference between the two groups (p = 0.369, p = 0.310 and p = 0.494 respectively). Although after treatment in both groups symptom score and endoscopy score were significantly improved but not the CT score, we found no difference in between the groups at sixth month. In most of the previous studies, patients with CRSwE-NP were assumed to have poor prognosis and high recurrence rate despite surgical or medical treatment. However, we did not find any association between eosinophilic or neutrophilic nature of nasal polyp tissue and disease severity.

Investigation of neuroprotective and therapeutic effects of cannabidiol in an acute coronary syndrome model.

PURPOSE: The ischemia-reperfusion (I/R) injury seen in the heart can cause severe damage to essential organs such as the brain. Cannabidiol (CBD) obtained from Cannabis sativa is used today to treat various diseases. This study aimed to demonstrate CBD's neuroprotective and therapeutic properties in rats with brain damage caused by I/R in the heart. MATERIALS: Rats were divided into four groups; sham, I/R, I/R + Prophylactic CBD, and I/R + Therapeutic CBD. End of the experiment, brain tissues were collected for biochemical, histopathological, and genetic examinations. RESULTS: I/R damage increased the number of degenerative neurons, caspase-3 and TNF-α immunoexpression, total oxidant status levels, and oxidative stress index. Both prophylactic and therapeutic CBD administration reduced these increased values. In addition, the relative fold changes of AMPK, PGC-1α, SIRT1, and Bcl 2 decreased in the I/R group, and the relative fold change of Bax increased, which are indicators of ER stress and apoptosis. Both administrations of CBD reversed these genes' relative fold changes. CONCLUSION: CBD can be protective against brain injury caused by cardiac I/R damage through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms.

Management of patients with coexisting obstructive sleep apnea and laryngopharyngeal reflux disease.

Obstructive sleep apnea syndrome (OSAS) and Laryngopharyngeal reflux disease (LPR) are both common health problems causing severe morbidity. Since they have similar risk factors, the prevalence of LPR among patients with OSAS is higher compared with general population. However, there exist only a few studies showing the potential causal relation between LPR and OSAS. The aim of this study was to evaluate the coexistence between OSAS and LPR and to determine whether the therapy of OSAS alters LPR parameters and vice versa. In this study, 44 patients underwent double probed 24 h pH monitoring simultaneously with polysomnography due to the complaints of obstructive sleep apnea and reflux. Twenty of those 44 patients were diagnosed with both OSAS and LPR. Among those patients, 10 patients with mild to moderate OSAS were given only LPR treatment for 3 months. The remaining 10 patients who had severe OSAS underwent CPAP treatment for 3 months. After the end of treatment, all patients were reevaluated with double probed 24 h pH monitoring simultaneously with PSG. Moreover, the patients were evaluated subjectively by Epworth Sleepiness Scale (ESS), snoring Visual Analogue Scale (VAS), Reflux Symptom Index (RSI), and Reflux Finding Score (RFS). The results of this study revealed that OSAS and LPR coexist frequently. LPR treatment did not improve the polysomnographic parameters, but significantly reduced ESS and snoring VAS (p = 0.02 and p = 0.007, respectively). Although the CPAP treatment significantly improved subjective parameters of reflux, such as RSI and RFS (p = 0.016 for both), there was no significant improvement in objective parameters of 24-h pH monitoring. We concluded that since there is a high frequency of coexistence between LPR and OSAS, all patients with OSAS should also be queried for LPR symptoms. In addition, more in-depth and comprehensive research is required to elucidate the association between OSAS and LPR.

Haplotype variation of estrogen receptor-alpha (ER-alpha) gene exon 4 in Turkish sheep breeds.

Estrogen receptor a (ERalpha) gene has previously been found to related with sexual development and reproduction. In this study, on the basis of the sequences of human, cattle and caprine estrogen receptor a (ERalpha) genes, available in the GenBank database, sets of PCR primers were designed and used to amplify the ovine ERalpha gene exon 4 region. We identified six single nucleotide polymorphisms (SNP) in the ERalpha exon 4. Some variations determined for exon 4 g.43A > G, p.T43A; g.49C > T, p.L49F; g.178A > T, p.T178S led to changes in the amino acids, but no amino acid changes were determined in g. 18G > C, g.27C > T, g.96G > A. These fragments were deposited in the GenBank database under accession number: JF262030-JF262035. It was noted in particular that White Karaman and Awassi breeds were similar to each other, whereas the Chios breed had a different variation.

Erratum to: Evaluation of the Effects of Favipiravir Combined with Vitamin C on Alveolar Bone in Rats.

[This corrects the article DOI: 10.1134/S0022093022020119.].

Evaluation of the Effects of Favipiravir Combined with Vitamin C on Alveolar Bone in Rats.

Introduction: Favipiravir and Vitamin C (Vit C) were used together in the treatment of the COVID-19 pandemic. However, the effects of favipiravir on the periodontium are still unknown. Therefore, the aim of this study was to investigate the effects of Favipiravir and Vit C treatment on alveolar bone metabolism. Experimental: Fifty healthy adult male Sprague-Dawley rats (2-3 months old) were randomly divided into five equal groups (n = 10): Control, Favi 20, Favi 100, Favi 20+Vit C, Favi 100+Vit C. Favipiravir (20 mg/kg and 100 mg/kg, i.m.) and Vit C (150 mg/kg/day, oral) were administered to the rats for 14 days. Alveolar bone loss (ABL) and histopathological changes were examined using a light microscope. Immunohistochemistry was used to determine levels of receptor activator of nuclear factor kappa-B ligand (RANKL), caspase-3, bone morphogenic protein 2 (BMP-2) and alkaline phosphatase (ALP) in the bone tissues. Results: Favipiravir increased the levels of RANKL and caspase-3 expression but decreased BMP-2 and ALP levels in a dose-dependent manner. Favi 20+Vit C and Favi 100 +Vit C groups showed decreased RANKL and caspase-3 levels in addition to increased BMP-2 and ALP levels. Conclusion: Favipiravir can cause histopathological damage to the periodontium, but administration of favipiravir combined with Vit C can provide a protective effect against this damage.

Apigenin alleviates methotrexate-induced liver and kidney injury in mice.

Methotrexate (MTX) is a drug used in the treatment of various types of cancer and inflammatory diseases, but its clinical use has been restricted due to its toxicity. Apigenin (API) is an effective flavonoid with antioxidant and anti-inflammatory properties. The aim of this study was to determine the protective effect of API against MTX-induced liver and kidney toxicity. Four groups with 12 male mice each were used. The control and API groups were received 0.9% saline (ip) and API (3 mg/kg ip) for 4 days, respectively. The MTX group were given a single dose of MTX (20 mg/kg ip) on the fourth day. The MTX + API group were administered API for 7 days and then MTX on fourth day. Blood, liver and kidney were collected to evaluate tissue injury markers, oxidative stress biomarkers, and histopathological and immunohistochemical assessments. In MTX-treated group, significant increases in aminotransferases activities, creatinine and malondialdehyde (MDA) levels and significant decreases in catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase1 (SOD1) activities and glutathione (GSH) levels were determined compared to the control group. Furthermore, histopathological changes and significant increases in caspase-3, C-reactive protein (CRP), granulocyte colony-stimulating factor (G-CSF), and inducible nitric oxide synthase (iNOS) expressions were detected in both liver and kidney tissues of MTX-treated mice. Pretreatment with API alleviates liver and kidney toxicity by attenuating oxidative stress and tissue injury markers, histopathological alterations, and apoptosis and inflammation. These results suggest that API has a protective effect against oxidative stress and liver-kidney toxicity induced by MTX.

The Effect of Pre-emptive Dexketoprofen Administration on Postoperative Pain Management in Patients with Ultrasound Guided Interscalene Block in Arthroscopic Shoulder Surgery.

Background: Postoperative pain is an important problem for patients undergoing shoulder surgery. Our study investigated analgesic efficacy, duration of analgesia, postoperative analgesic use and patient satisfaction with the use of preemptive intravenous dexketoprofen for interscalene block in addition to general anesthesia in arthroscopic shoulder surgery. Methods: 60 patients, scheduled for arthroscopic shoulder surgery were randomized (30 patients each) into either: - control group (Group1) or dexketoprofen group (Group 2). Patients were followed for 48 hours to compare both groups for; post-operative pain scores, effectiveness of postoperative analgesia, duration of analgesia, and analgesia consumption. Duration of postoperative sensory block of the shoulder joint was defined as time to onset of pain at the incision site. Duration of postoperative motor block of the shoulder joint was defined as time to onset of first shoulder movement. Results: While no significant difference was determined for motor block time, sensory block time was significantly longer in the dexketoprofen group (p < 0.05).VAS scores were significantly lower at all times in the dexketoprofen group (p < 0.05).Total PCA fentanyl consumption was 274.16 ± 314.89 (µg) in the dexketoprofen group, and 490.00 ± 408.98 (µg) in the control group, the difference was statistically significant (p < 0.05). No significant difference was observed between the groups' demographic and hemodynamic data. Conclusion: Pre-emptive IV dexketoprofen may be a good option for arthroscopic shoulder surgery and provides effective analgesia.

Ameliorative effects of pregabalin on LPS induced endothelial and cardiac toxicity.

We investigated the antioxidant, anti-inflammatory and anti-apoptotic effects of pregabalin (PREG) on lipopolysaccharide (LPS) induced sepsis related cardiotoxicity via NF-kß pathways. We used 24 female Wistar albino rats divided into three groups: control, LPS treated and LPS + PREG treated. Total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), tumor necrosis factor alpha (TNF-α), nuclear factor kappa beta (NF-kß)/p65, p-NF-kß/p65, caspase-3 (Cas-3) and cleaved Cas-3 were measured in cardiac tissues and creatine kinase MB (CKMB), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) levels were measured in blood samples. Also, Cas-3, granulocyte-colony stimulating factors (G-CSF), interleukin-6 (IL-6), serum amyloid A (SAA) and inducible nitric oxide synthase (iNOS) were measured immunohistochemically in heart and aorta tissue. In the LPS group; the levels of CKMB, AST, LDH, TOS, OSI increased and TAS decreased. TNF-α, p-NF-kß/p65 and Cas-3 protein levels also increased in the LPS group. Immunohistochemical evaluation of the heart and aorta revealed a significant increase in the levels of Cas-3, G-CSF, SAA, IL-6 and iNOS in the LPS group. PREG treatment restored all measurements to near normal. LPS induced cardiovascular toxicity was due to inflammation, oxidative stress and apoptosis. PREG ameliorated the damage by inhibition of NF-kß phosphorylation.

Examination of skin lesions in rats with induced hyperthyroidism and hypothyroidism.

We investigated the pathogenesis of skin lesions due to hypothyroidism and hyperthyroidism in rats. We used 30 rats allocated into hypothyroidism, hyperthyroidism and control groups. Blood samples were evaluated for levels of thyroid stimulating hormone (TSH), tri-iodothyronine (T3) and thyroxine (T4). Skin samples were examined for melan-A, lymphatic vessel endothelial hyaluronic acid receptor 1 (LYVE1), cluster of differentiation 31 (CD31), protein gene product 9.5 (PGP9.5), calretinin, chromogranin, synaptophysin and pancytokeratin. Histopathological examination of the skin sections revealed thickened epidermis in the hyperthyroidism group due to an increased number of cells, and a decreased number of hair follicles and epithelial cell rows in the epidermis with an increased number of fat cells in the dermis of the rats in the hypothyroidism group. No significant difference was observed in the immunoreactions of pancytokeratin, PGP9.5, CD31 and synaptophysin among the groups. The hyperthyroidism and hypothyroidism groups exhibited a marked increase in melan-A immunoreaction. Expression of LYVE-1, chromogranin and calretinin was increased in the hyperthyroidism group and decreased in the hypothyroidism group. We found that melan-A, LYVE-1, chromogenin and calretinin play an important role in the pathogenesis of skin lesions caused by thyroid disorders.

Artemisinin attenuates doxorubicin induced cardiotoxicity and hepatotoxicity in rats.

We investigated the effects of artemisinin on doxorubicin (Dox) induced heart and liver pathology in rats. We divided 49 male rats into seven groups: group 1 was the untreated control. Dox was administered intraperitoneally to groups 2, 3 and 4 on day 1. Artemisinin was administered by gavage to groups 3 and 6 at a dose of 7 mg/kg, and to groups 4 and 7 at a dose of 35 mg/kg for 14 days. Group 5 was given only 0.9% NaCl orally for 14 days. At the end of the study, heart and liver samples were collected for histopathology and immunohistochemistry. Hyperemia and slight hemorrhages were observed in both livers and hearts of rats treated with Dox only. Significant increases in caspase-3, TNF-α, iNOS and NF-κB expression were observed in the myocardial cells and hepatocytes of group 2. Significant reductions in caspase-3, TNF-α, iNOS and NF-κB expression were observed in groups 3 and 4 following artemisinin treatment compared to group 2. Artemisinin may exert protective effects against Dox induced cardiotoxicity and hepatotoxicity in rats.

Effects of alpha-lipoic acid on high fructose induced hepatic pathology.

Little is known about the pathogenesis of high fructose corn syrup (HFCS) induced hepatic toxicity. We investigated hepatic lesions induced by chronic HFCS consumption and the protective effects of alpha-lipoic acid (ALA) on liver pathology. We used 24 rats allocated randomly into three groups of eight. The HFCS group was given in drinking water for 10 weeks. The ALA + HFCS group was given the same dose of HFCS and ALA also was administered during the last 6 weeks of the experiment. The control group was untreated. The rats were euthanized at the end of 10 weeks and 24 h after the last ALA administration. A significant increase was observed in the serum aspartate aminotransferase (AST) level of the HFCS group compared to controls. Tissue malondialdehyde (MDA) levels also increased significantly and catalase (CAT) activity decreased significantly in the HFCS group. Caspase-3 expression increased significantly in the HFCS group compared to controls. In the ALA treated group, the levels of MDA, CAT and caspase-3 returned to near control levels. HFCS caused hepatic toxicity by increasing oxidative stress and apoptosis. ALA administration ameliorated the pathological changes.