Efficacy of butterbur in allergic rhinitis: a cell culture study.

OBJECTIVE: The study aims to define butterbur's impact on nasal cells' viability and proliferation. After topically administering butterbur to the nasal epithelial cells, research has been done to see if butterbur has any harmful effect on the nasal cells. MATERIALS AND METHODS: Specimens of healthy primary nasal epithelium were collected from the subjects and incubated in cell culture in due course of septoplasty. After implementing 2.5 µM butterbur in cultured cells, cell viability was defined via trypan blue assay, and proliferation was defined via the XTT method. The number of total cells, viability, and proliferation was defined. XTT (2, 3-bis-(2-methoxy-4-nitro-5-sulphophenyl)-2H-tetrazolium-5-carboxanilide) experiments can be used to evaluate cellular toxicity. RESULTS: The findings of the XTT experiment reveal no harm to nasal cells after topical implementation of butterbur. No significant change in the proliferation of the cells, no matter what the doses are. There was no cytotoxic effect on the primary nasal cells at the end of 24 hours of implementation, and no side effects were found. There was no difference in cells' viability between the experimental group with butterbur application and the control group. CONCLUSIONS: Cytotoxicity on nasal cells was not observed after the butterbur application. Even if there have been some indications of liver toxicity, butterbur can be suggested as a safe option for seasonal allergic rhinitis. Further studies related to the toxicity of topical butterbur are also recommended, even though this study indicates no cytotoxicity from the topical application on nasal cells.

Is tannic acid a promising option in local treatment of nasal diseases?

OBJECTIVE: We investigated the effects of tannic acid on viability and proliferation of nasal cells after topical application. It was also evaluated whether tannic acid served as an alternative treatment agent. MATERIALS AND METHODS: Collected primary nasal epithelium from healthy people who had undergone septoplasty operations were incubated in cell culture. Following the implementation of 2.5 µM tannic acid in cultured cells, both the number of total cells and their viability were measured using the trypan blue assay, while proliferation was assessed through the XTT method. The XTT method, which involves using "2,3-bis-(2-methoxy-4-nitro-5-sulphophenyl)-2H-tetrazolium-5-carboxanilide", is a reliable means of determining cellular toxicity. RESULTS: XTT experiment results showed that there was no harm was detected to nasal cells after tannic acid's topical implementation. There were no significant changes in cell proliferation; moreover, no matter what the doses were. Additionally, no cytotoxic effects were detected on nasal cells' primary culture at "the end of the 24 hours of implementation". There was no side effect of it, either. CONCLUSIONS: According to the research, the application of tannic acid topically did not result in any harmful effects on the nasal cell culture. Tannic acid's potential anti-inflammatory properties and its ability to decrease Th2-related cytokines suggest that it may be beneficial for patients with rhinosinusitis or allergic rhinitis, pending confirmation through clinical trials. Additionally, if clinical trials confirm its effectiveness, tannic acid may be useful in healing wounds for patients undergoing septorhinoplasty.

Investigation of the effect of the curcumin component as an alternative to the local treatment of nasal diseases.

OBJECTIVE: This study aimed to define the impacts of curcumin on nasal cell viability and proliferation. MATERIALS AND METHODS: Specimens of healthy primary nasal epithelium were collected and incubated in cell culture during septorhinoplasty from people who signed a consent form. After implementing 2.5 µM curcumin in cultured cells, cell viability was defined via trypan blue assay, and proliferation was defined via the XTT method. The number of total cells, viability, and proliferation was defined. XTT (2,3-bis-(2-methoxy-4-nitro-5-sulphophenyl)-2H-tetrazolium-5-carboxanilide) experiments can be used to evaluate cellular toxicity. RESULTS: The results revealed no harm to nasal cells after the topical implementation of curcumin. There was no significant change in the proliferation of the cells related to 24 hours of implementation. There was no adverse effect of using curcumin on the cell viability, either. CONCLUSIONS: No cytotoxic effect on nasal cells has been observed after applying topically implemented curcumin. Curcumin could be used topically for an alternative treatment for allergic rhinitis as it has anti-inflammatory and immune response modulatory effects if clinical trials will confirm experimental data.

Inhibition of voltage­gated potassium channels affect expressions of miR-126 and miR-126* in breast cancer cell lines.

AIM: We aimed to determine the possible correlation between voltage­gated potassium channels and micro RNAs in breast cancer and metastatic breast cancer cells. METHOD: Kv1.3 and Kv10.1 channels were inhibited by specific siRNAs using a lipofectamine-based transfection in MCF-7 and MDA-MB-231 cells. After transfection, total RNA was isolated, and then miR-126 and miR-126* expressions were observed using RT-PCR. RESULTS: There was a negative correlation between Kv channels and miRNAs according to the characteristics of the breast cancer cells. The inhibition was observed not only in Kv1.3 but also in Kv10.1 in MCF-7 cells, and miR-126 and miR-126* expressions were downregulated compared to the control group (p < 0.001). The inhibition of these channels in MDA-MB-231 cells caused an upregulation of miR-126 and miR-126* expressions (p < 0.001). CONCLUSION: The miR-126 and miR-126* expressions differed according to benign and malign breast cancer cell lines. Furthermore, we found that miR-126/126* may interact with Kv1.3 and Kv10.1 voltage-gated potassium channels. Our study suggests and indicates the relationship between Kv channels and miRNAs in breast cancer cells (Tab. 1, Fig. 2, Ref. 51).

Tannic acid exhibits anti-inflammatory effects on formalin-induced paw edema model of inflammation in rats.

The aim of the study was to determine the relationship between anti-inflammatory effects of the natural polyphenolic compound tannic acid (CAS number: 1401-55-4) and myeloperoxidase (MPO) enzyme activity in paw edema model. Thirty-five female rats were divided into five groups. The paws of rats were injected subcutaneously in the plantar surface with formalin except for the control group. Indomethacin and tannic acid were intraperitoneally administered 1 h after formalin injection. The paws volume was measured by using vernier caliper. MPO enzyme activity was determined using 4-aminoantipyrine-phenol solution as the substrate for MPO-mediated oxidation by H2O2. About 17% and 13% edema inhibition has detected in the indomethacin-applied group, at the measurements run every other hour right after the treatment. An inhibition of 16% was found at the group treated with 25 mg/kg tannic acid. However, in the group treated with 50 mg/kg tannic acid, 15% and 7% of the edema inhibition was observed. Serum and paw tissue MPO activities were decreased in treated groups with indomethacin and tannic acid according to formalin control group. Our study results suggest that tannic acid may contribute to the treatment of inflammation by decreasing MPO enzyme activity, but the molecular mechanism is still not clear.

Micro RNA-126 coordinates cell behavior and signaling cascades according to characteristics of breast cancer cells.

BACKGROUND: Micro RNA-126 is known to enhance apoptotic processes and also plays a role in vascular growth through the regulation of vascular endothelial growth factor-mediated signaling, angiogenesis, and vascular integrity. OBJECTIVES: We aimed to determine the role of miR-126 in breast cancer cell lines with a variety of different characteristics to evaluate its interaction with certain cancer-related molecules and mechanisms. METHODS: To determine the effect of presence and absence of miR-126 in MCF-7 and MDA-MB-231 breast cancer cells, miR-126 mimics and inhibitor were transfected. miRNA and gene expressions were observed by using RT-PCR. Viability, proliferation, adhesion, invasion and lateral motility assays were performed to determine cell behavior changes. RESULTS: miR-126 is more effective on MDA-MB-231 cells on cell behavior. We observed an increase in miR-126 expression when miR-126 mimics was transfected to MCF-7 and MDA-MB-231 cells. Also, there was a decrease in miR-126 expression when MCF-7 and MDA-MB-231 cells were transfected with miR-126 inhibitor. Furthermore, presence and absence of miR-126 modulated the gene expressions of VEGF/PI3K/AKT and MAPK signaling in MCF-7 and MDA-MB-231. CONCLUSION: Our study showed that miR-126 is in a state of interaction with a multitude molecules playing a role in breast cancer. According to obtained data, we can say that miR-126 may be more effective in inhibition of metastatic breast cancer (Tab. 4, Fig. 3, Ref. 46).

Effect of etanercept and lithium chloride on preventing secondary tissue damage in rats with experimental diffuse severe brain injury.

OBJECTIVE: Studies in animals have provided key evidence that antagonizing TNF-α is a viable therapeutic strategy for diffuse severe brain injury. This study is planned to prevent post-traumatic secondary tissue damages in rat diffuse severe brain injury model, which is induced by alone or combined administration of Etanercept and lithium chloride (LiCl). MATERIALS AND METHODS: Male Sprague-Dawley rats were used in the current study. Rats were divided into 5 groups. Trauma was not induced and treatment was not applied to rats of Sham group. For rats of Trauma+Saline group, saline 0.9% was administered via intraperitoneal (i.p.) route at dose of 1 mg/100 g body weight 1 hour after trauma. For rats of Trauma+Etanercept group, Etanercept was administered via i.p. route at dose of 5 mg/kg body weight 1 hour after trauma. For rats of Trauma+LiCl group, LiCl was administered via i.p. route at dose of 50 mg/kg body weight 1 hour after trauma. For rats of Etanercept+LiCl group, Etanercept and LiCl were administered via i.p. route at dose of 5 mg/kg body weight and 50 mg/kg body weight, respectively, 1 hour after trauma. Serum glial fibrillary acidic protein (GFAP) and Tau levels were analyzed with ELISA. For analyses H&E, TUNEL, GFAP and TNF-α staining methods were used. RESULTS: We demonstrate that Etanercept treatment reduced the TBI-induced brain tissues alteration, reduced the expression of TNF-α and improve edema and axonal swelling. We observed a significant decrease in TNF-α and GFAP positivity after LiCl was administered. CONCLUSIONS: The findings obtained in this study suggest that the combination therapy with Etanercept and LiCl decreased neuronal degeneration and alleviated secondary tissue damage in post-traumatic period.

Investigation of the course of GFAP in blood in the initial 24 hours in rats subjected to minor head trauma.

AIM: Aim of this study is to evaluate the diagnostic efficacy of Glial Fibrillar Acidic Protein (GFAP) particularly in minor head traumas. MATERIALS AND METHODS: 72 female and male, 3 month-old, Sprague Dawley rats were used in the study. The rats were divided into 9 groups. Following anesthesia, all rats were placed in prone position. A 10 mm long and 3 mm thick stainless steel metal disc was fixed onto the skull using dental paste in order to sustain a closed head trauma and evenly distribute the weight throughout the skull. After placing it under the metallic pipe arrangement over a height of 80 centimeters and fixing to make it constant, 50 g metallic discs were released by free fall, and the head trauma was sustained thanks to the gravity-generated force. Blood samples were collected from the rats under anesthesia for biochemical GFAP analysis 10 minutes after the trauma and in 1, 2, 3, 4, 5, 6 and 24 consecutive hours later. RESULTS: GFAP has a peak, and its peak level at hours 1 and 2 in rats subjected to a minor head trauma, with a slight decrease afterwards. CONCLUSIONS: GFAP is an important marker in determining the severity of traumatic brain injury.

Trace minerals in experimental subarachnoid haemorrhage: zinc, copper and manganese levels in rat brain tissue, blood and urine.

BACKGROUND: Zinc (Zn), copper (Cu) and manganese (Mn) are involved in regulatory systems in the cell. Their role in neuromodulator activities and redox reactions has been implicated in the pathogenesis of neurological disorders. The aim of this study was to determine changes of Zn, Cu and Mn levels in brain tissue, blood and urine after experimental subarachnoid haemorrhage (SAH). The possible importance of these trace minerals on the pathogenesis of SAH was also discussed. METHOD: Rats were divided into three groups; namely a SAH group, a control group and a normal group. Blood samples in the SAH group and normal saline in the control group were injected into the cisterna magna. No surgical procedures were performed on the normal group. Brain tissue, blood and urine samples were measured for trace minerals by atomic absorption spectrophotometry. Measurements were taken on days 3, 7 and 10 after the onset in the control and SAH groups, and on the first day in the normal group. FINDINGS: The reduced blood Zn levels and increased Zn urine loss observed in the SAH group were conspicuously significant. Furthermore, significant changes in Mn levels were also seen at different stages of the trial in the SAH group. However, differences found in the Cu levels between the groups were not significant enough to explain the results. INTERPRETATION: These results suggest that the low blood Zn levels seen throughout the stages, the low brain tissue Mn levels seen during the latter part of the trial, and the low blood Mn levels observed during the early stages, may all be related to an increased risk in experimental SAH in rats. These differences may have possible role in the pathogenesis of SAH, and further investigations into the reduced blood Mn levels observed during the study may lead to new insight into the treatment of SAH.