مجله علوم پایه پزشکی ایران
سال:1397 | دوره: | شماره: |تعداد مقالات:15

Objective(s): Periodontal diseases are among prevalent oral health problems which may ultimately lead to severe complications in oral cavity. Herbal products can be designed as single or multicomponent preparations for better oral health. This study aims to review current clinical trials on the effectiveness of herbal products in gingivitis. Materials and Methods: Electronic databases, including PubMed, Scopus, ScienceDirect and Cochrane library were searched with the keywords “ gingivitis” in the title/abstract and “ plant/ extract/ herb” in the whole text for clinical trials on herbal treatments for gingivitis. Data were collected from 2000 until January 2018. Only papers with English full-texts were included in our study. Results: Herbal medicines in the form of dentifrice, mouth rinse, gel, and gum were assessed in gingivitis via specific indices including plaque index, bleeding index, microbial count, and biomarkers of inflammation. Pomegranate, aloe, green tea, and miswak have a large body of evidence supporting their effectiveness in gingivitis. They could act via several mechanisms such as decrease in gingival inflammation and bleeding, inhibition of dental plaque formation, and improvement in different indices of oral hygiene. Some polyherbal formulations such as triphala were also significantly effective in managing gingivitis complications. Conclusion: Our study supports the efficacy and safety of several medicinal plants for gingivitis; however, some plants do not have enough evidence due to the few number of clinical trials. Thus, future studies are mandatory for further confirmation of the efficacy of these medicinal plants.

Objective(s): The study explored the neuroprotective role of Kalirin-7 (Kal-7) in Neuro-2A cells after oxygen-glucose deprivation and reperfusion (OGD/R) treatment. Materials and Methods: The study used an OGD/R model of mouse Neuro-2A neuroblastoma cells in vitro. Cells were transfected with pCAGGS-Kal-7 to up-regulating kal-7. Then cell proliferation and apoptosis were respectively analyzed by Trypan blue exclusion method and flow cytometry. To examine the involvement of Rac1, cells were treated with Rac1-GTP inhibitor NSC23766 before treatment with OGD/R. Expressions of Bax, Bcl-2, Rac1, and down-stream targets of Rac1 were analyzed by Western blot. Results: Kal-7 significantly decreased OGD/R induced cell apoptosis (P<0. 01), but no significant effects were observed on cell proliferation. Kal-7 increased the expressions of apoptosis-related protein of Bcl-2 and Rac1, but decreased the expression of Bax in Neuro-2A cells stimulated to OGD/R. Rac1 was activated by Kal-7 due to the increased levels of its down-stream targets, p-p38 and p-PAK1. NSC23766 reduced the anti-apoptotic effect of Kal-7 as the enhanced apoptotic cell rate and increased Bax/Bcl-2 ratio. Conclusion: These findings suggest that the protective effects of Kal-7 against OGD/R injury in Neuro-2A cells were dependent in a Rac1 activation signaling.

Objective(s): According to recent the findings, sulfur dioxide (SO2) is produced by the cardiovascular system, influencing some major biological processes. Based on previous research, SO2 exhibits antioxidant effects and inhibits apoptosis following cardiac ischemia/reperfusion. Therefore, the objective of the current study was to examine the neuroprotective impact of SO2 following global cerebral ischemia/reperfusion (I/R). Materials and Methods: Forty-eight male Wistar rats that weighed 260– 300 g, were randomly allocated into 4 groups: sham group (n=12), I/R group (n=12), and I/R+SO2 groups (NaHSO3 and Na2SO3; 1: 3 ratio; 5 and 10 μ g/kg, respectively; for 3 days, n=12). Cerebral ischemia model was prepared by occlusion of both common carotid arteries for 20 min. Saline as a vehicle and SO2 donor at doses 5 μ g/kg (intraperitoneally) were injected for 3 days after reperfusion. Four days after ischemia, the passive avoidance memory test was carried out in four groups, and after behavioral assessment, necrosis, apoptosis, and antioxidant enzyme analysis were carried out. Results: SO2 treatment could significantly improve memory impairments in rats with cerebral ischemia/reperfusion (I/R) (P<0. 05). An increase in both superoxide dismutase and glutathione and a reduction in malondialdehyde were reported in the SO2 group versus the ischemic group (P<0. 05). Moreover, SO2 could significantly decrease necrotic and apoptotic cells in the CA1 region (P<0. 01). Conclusion: According to the findings, SO2 exerts significant neuroprotective effects on cerebral I/R due to its antioxidant activity.

Objective(s): The beneficial outcomes of bone marrow-derived mesenchymal stem cell (BMSC) treatment on functional recovery following stroke has been well established. Furthermore, 5-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors have also been shown to increase neuronal survival and promote the movement of BMSCs towards the sites of inflammation. However, the precise mechanisms mediating the improved neurological functional recovery in stoke models following a combination treatment of Simvastatin and BMSCs still remained poorly understood. Materials and Methods: Here, an embolic stroke model was used to experimentally induce a focal ischemic brain injury by inserting a preformed clot into the middle cerebral artery (MCA). Following stroke, animals were treated either with an intraperitoneal injection of Simvastatin, an intravenous injection of 3 ×106 BMSCs, or a combination of these two treatments. Results: Seven days after ischemia, the combination of Simvastatin and BMSCs led to a significant increase in BMSC relocation, endogenous neurogenesis, arteriogenesis and astrocyte activation while also reducing neuronal damage when compared to BMSC treatment alone (P<0. 001 for all). In addition, based on western blot analysis, following stroke there was a significant decrease in c-Fos expression (P<0. 001) in the combination treatment group. Conclusion: These results further demonstrate the synergistic benefits of a combination treatment and help to improve our understanding of the underlying mechanisms mediating this beneficial effect.

Objective(s): The purpose of this study was to detect the protective effects of adiponectin on coagulation dysfunction and its mechanism in sepsis of rats. Materials and Methods: The experimental samples were composed of sham group, model group that was underwent cecal ligation and puncture (CLP) and three adiponectin treatment groups that treated by adiponectin with different dose (72 μ g/kg, 96 μ g/kg and 120 μ g/kg) after CLP. The prothrombin time (PT), activated partial thromboplastin time (APTT) was measured, respectively, the level of malondialdehyde (MDA), tissue factor (TF), activated coagulation factor VIIa and Xa, p-selectin were detected, the histology structure of vascular was observed, the expressions of Caspase 9, Caspase 3, Bax, Bcl-2 and vWF in vascular were measured. Results: The results demonstrated that adiponectin treatment lengthened PT and APTT, reduced the expression of MDA, TF, activated coagulation factor VIIa, Xa and p-selectin in plasma of septic rats. Additionally, adiponectin treatment alleviated endothelial cell apoptosis and oxidative stress, downregulated the levels of Caspase 3, Caspase 9, Bax, Bcl-2 and vWF in vascular. Conclusion: These findings suggest that adiponectin treatment might be a promising therapeutic strategy for relieving septic endothelial cell injury and coagulation dysfunction via inhibiting endothelial cell apoptosis in septic rats.

Objective(s): Dehydroepiandrosterone (DHEA) has been reported to improve pregnancy chances in women with diminished ovarian reserve (DOR) and to reduce miscarriage rates by 50– 80%. This study, therefore, assesses effects of DHEA on number of retrieved oocytes and meiotic spindles. Materials and Methods: A randomized, prospective, controlled study was conducted on eight groups, four groups of young mice and four elderly. All young and old groups received different oral doses (35, 50, 75 mg/kg) of DHEA for 3 months. Meiotic spindle assessment was done by immunocytochemical techniques using a confocal laser microscope (Leica TCS-4D). Results: Statistical surveys showed that in control young groups 80% (P=0. 0845) and in the old control group 73. 3% (P=0. 000) of the meiotic spindles have a normal shape and structure; the difference was meaningful. The young with 50 mg/kg of DHEA in 85. 4% and the young with 75 mg/kg of DHEA in 84. 2% were normal in shape and structure. Statistical analysis showed that the difference was meaningless (P=0. 845). The old group with 30 mg/kg of DHEA in 81. 1%, the old with 50 mg/kg of DHEA in 83. 9%, and the old with 75 mg/kg of DHEA in 79. 0% showed normal shape and structure. The meiotic spindle disruption ratio in old mice showed a significant difference (P=0. 000) in comparison with others in young groups. Statistical analysis showed that difference between DHEA and control groups is meaningful. But this difference was meaningless between DHEA groups. Conclusion: Results showed that DHEA has a positive and improvement effect on the meiotic spindle in old mice.

Objective(s): Diabetes mellitus (DM) is a widespread metabolic disorder worldwide. Clinical physicians have found diabetic patients have mild to middle cognitive dysfunction and an alteration of brain monoaminergic function. This study explored the change in various patterns of behavioral models and brain monoamine function under streptozotocin (STZ)-induced type 1 diabetes. Materials and Methods: We established a type 1 DM model via intravenous injection with STZ (65 mg/ kg) in rats. Three weeks after the STZ injection, various behavioral measurements including the inhibitory avoidance test, active avoidance test and Morris water maze were conducted. Finally, all rats were dissected and the concentrations of monoamines and their metabolites in cortex and hippocampus were measured by high performance liquid chromatography with electrochemical detection. Results: We found that STZ induced type 1 diabetes (hyperglycemia and lack of insulin) in rats. STZinduced diabetic rats had cognitive impairment in acquisition sessions and long-term retention of the active avoidance test. STZ-induced diabetic rats also had cognitive impairment in spatial learning, reference and working memory of the Morris water maze. STZ significantly reduced concentrations of norepinephrine (NE) in the cortex and dopamine (DA) in the hippocampus, but increased concentrations of DA and serotonin (5-HT) in the cortex 35 days after injection. The concentration of 5-HT in the hippocampus was also significantly increased. Conclusion: The data suggested that this cognitive impairment after a short-term period of STZ injection might be related to cortical NE dysfunction, differential alteration of cortical and hippocampal DA function, and brain 5-HT hyperfunction.

Objective(s): Chronic hyperglycemia leads to activation of the advanced glycation end products (AGE)-receptor (RAGE) for AGE axis and oxidative stress, which promote diabetic renal damage. This study examines the effect of insulin-loaded trimethyl chitosan nanoparticles on the kidney tissue of diabetic rats. Materials and Methods: Twenty-five male Wistar rats were randomly divided into 5 groups: normal control (C), diabetic group without treatment (DM), diabetic group treated with chitosan-based nanoparticle (DM+NP, 1 ml by gavage), diabetic group treated with 8 IU/kg insulin-loaded trimethyl chitosan nanoparticles (DM+N. in, 1 ml by gavage), and diabetic group treated with 8 IU/kg trade insulin (DM+SC. in, 0. 2 ml by subcutaneous injection). The animals were treated from weeks 8 to 10. At the end of the study, serum urea, creatinine, and uric acid were measured. Also, the level of AGE and RAGE mRNA expression, and oxidative stress markers were studied in the kidney tissue. Results: Insulin-loaded nanoparticles similar to trade insulin could significantly reduce urea, creatinine, and uric acid parameters, while the elevated total antioxidant capacity (TAC), thiol groups, and catalase activity also reduced total oxidant status (TOS) and malondialdehyde (MDA) levels (P<0. 05). However, the reduction in AGE and RAGE mRNA expression is not statistically significant in both treatments. Of course, the influence of insulin-loaded trimethyl chitosan nanoparticles on the amelioration of all these parameters is higher compared to that of the injected form. No markedly significant differences were observed between these two kinds of treatments. Conclusion: This data reveals that insulin-loaded trimethyl chitosan nanoparticle is a better therapeutic approach than injected insulin.

Objective(s): The novel healing choices for handling of infections due to multidrug resistant Staphylococcus aureus are reguired. HAMLET has been reported to be able to sensitize bacterial pathogens to traditional antimicrobial agents. The aim was to assess wound healing activity of methicillin in presence of HAMLET in methicillin resistant S. aureus (MRSA) infected wounds. Materials and Methods: Fifty male rats were randomized into five groups of ten animals each. In CONTROL group, 0. 1 ml sterile saline 0. 9% solution was added to the wounds with no infection. In MRSA group, the wounds were infected with MRSA and only treated with 0. 1 ml the sterile saline (0. 9%) solution. In MRSA/HAMLET group, infected wounds were cured with HAMLET (100 μ g). In group MRSA/ Met, animals with infected wounds were cured with 0. 1 ml local use of 1 mg/ml methicillin. In MRSA/Met/HAMLET group, animals with infected wounds were cured with local use of 0. 1 ml solution of methicillin (1 mg/ml) and HAMLET (100 μ g). All test formulations were used for ten consecutive days, twice a day, beginning from first treatment. Results: Microbiological examination, planimetric, histological and quantitative morphometric studies, immunohistochemical staining for angiogenesis, determination of hydroxyproline levels and RT-PCR for Caspase 3, Bcl-2 and p53 showed that there was significant difference between animals in MRSA/Met/ HAMLET group compared to other groups (P<0. 05). Conclusion: HAMLET could make methicillin beneficial for handling of MRSA infected wounds and had the prospective effect to consider this harmless agent for local application.

Objective(s): Pioglitazone, an anti-diabetic agent, has been widely used to treat type II diabetes. However, the effect of pioglitazone on myocardial ischemia reperfusion injury (MIRI) is still unclear. Herein, the objective of this study is to learn about the regulation and mechanism of pioglitazone effects on oxygen glucose deprivation (OGD)-induced myocardial cell injury. Materials and Methods: A cellular injury model of OGD-treated H9c2 cells in vitro was constructed to simulate ischemic/reperfusion (I/R) injury. Then, various concentrations of pioglitazone (0, 2. 5, 5, 7. 5 and 10 μ M) were used for the treatment of H9c2 cells, and CCK-8, flow cytometry and western blot assays were performed to examine cell viability, apoptosis, and the protein levels of factors involved in cell cycle and apoptosis in OGD-treated cells. MiR-454 inhibitor was used to suppress miR-454 expression, and whether miR-454 was involved in regulating OGD-induced cell injury was studied. Two key signal pathways were examined to uncover the underlying mechanism. Results: OGD reduced cell proliferation and induced apoptosis in H9c2 cells (P<0. 05, P<0. 01 or P< 0. 001). OGD-induced injury was significantly attenuated by pioglitazone at the concentration of 5 μ M. Additionally, pioglitazone significantly up-regulated miR-454 expression in OGD-injured cells (P< 0. 05 or P< 0. 01). MiR-454 suppression declined the protective effect of pioglitazone on OGD-injured H9c2 cells (P<0. 05 or P< 0. 01). Besides, pioglitazone activated PI3K/AKT and ERK/MAPK pathways via upregulating miR-454. Conclusion: Pioglitazone protected H9c2 cells against OGD-induced injury through up-regulating miR-454, indicating a novel therapeutic strategy for treatment of MIRI.

Objective(s): Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities. Clinically, it is essential to limit the development of cognitive impairment after TBI. In the present study, the neuroprotective effects of gallic acid (GA) on neurological score, memory, long-term potentiation (LTP) from hippocampal dentate gyrus (hDG), brain lipid peroxidation and cytokines after TBI were evaluated. Materials and Methods: Seventy-two adult male Wistar rats divided randomly into three groups with 24 in each: Veh + Sham, Veh + TBI and GA + TBI (GA; 100 mg/kg, PO for 7 days before TBI induction). Brain injury was made by Marmarou’ s method. Briefly, a 200 g weight was fallen down from a 2 m height through a free-falling tube onto the head of anesthetized animal. Results: Veterinary coma scores (VCS), memory and recorded hDG-LTP significantly reduced in Veh + TBI group at 1 and 24 hr after TBI when compared to Veh + Sham (P<0. 001), respectively, while brain tissue content of interleukin-1β (IL-1β ), IL-6, tumor necrosis factor-α (TNF-α ) and malondialdehyde (MDA) were increased significantly (P<0. 001). Pretreatment of TBI rats with GA improved clinical signs, memory and hDG-LTP significantly (P<0. 001) compared to Veh + TBI group, while brain tissue content of IL-1β , IL-6, TNF-α and MDA were decreased significantly (P<0. 001). Conclusion: Our results propose that GA has neuroprotective effect on memory and LTP impairment due to TBI through decrement of brain lipid peroxidation and cerebral pro-inflammatory cytokines.

Objective(s): Newer organo-metallic, specifically gold (III) complexes with multiple ligands are currently being formulated with primary focus of having increased anti-cancerous properties and decreased cytotoxicity. In this study, histological toxicity profile of a newly formulated anticancerous gold (III) compound [trans-(± )-1, 2-(DACH)2Au]Cl3 Bis(trans-1, 2-Diaminocyclohexane) was investigated by evaluation of kidney and liver tissues of rats treated by the compound. Materials and Methods: This is a quasi-experimental study. In acute toxicity component of the study, (n = 16) male rats weighing between 200– 250 g were administered single, variable concentration of the gold (III) compound, [trans-(± )-1, 2-(DACH)2Au]Cl3 Bis(trans-1, 2-Diaminocyclohexane) to determine LD50 (dose that is lethal to 50% of rats). An IP injection of 2. 3 mg/kg (equivalent to 1/10 of LD50) was injected for 14 consecutive days to (n=10) male rats in the sub-acute component of the study. Autopsy preservation of liver and kidney tissue in buffered formalin, sample processing, histopathological evaluation, and comparison with unremarkable controls (n=5) was conducted sequentially. Results: A dose of 2. 3 mg/kg did not produce any tubular necrosis in kidney specimens. Mild interstitial inflammation with prominence of plasma cells was the main histological alteration. Plasmacytic pyelitis was also seen. Varying extents of cytoplasmic vacuolization and mild focal lobular and portal inflammation were predominant hepatic microscopic findings. Conclusion: [trans-(± )-1, 2-(DACH)2Au]Cl3 Bis(trans-1, 2-Diaminocyclohexane) produced no histological damage in renal and hepatic tissues of rats. This very limited sample animal-based study points to the relative safety of this new gold compound. However, there is a need to compare this compound with established drugs in a comparative non-animal based study.

Objective(s): Pathophysiology of sepsis-associated renal failure (one of the most common cause of death in intensive care units) had not been fully determined. The effect of nitric oxide and protein kinase C (PKC) pathways in isolated kidney of Lipopolysaccharide-treated (LPS) rats were investigated in this study. Materials and Methods: Vascular responsiveness to phenylephrine and acetylcholine in the presence and absence of a potent PKC inhibitor (chelerythrine) and nonspecific NO inhibitor (L-NAME) as well as responses to acetylcholine and sodium nitroprusside (SNP) were examined. Results: LPS (10 mg/kg, IP) treatment resulted in a lower systemic pressure and reduction of responses to vasoconstrictor and vasodilator agents (P<0. 05 to P<0. 01). The contractile response to phenylephrine and the relaxation response to acetylcholine were significantly blunted in isolated kidneys removed from LPS-treated rats. L-NAME (10 μ M) preincubation modified the responses to acetylcholine in isolated kidneys of control animal (P<0. 001) but not in LPS-treated rats. While, chelerythrine (10 μ M) preincubation partially restored response to phenylephrine in LPS-treated tissues. Conclusion: Present study highlighted that five hours of intraperitoneal endotoxin injection is adequate to reduce renal basal perfusion pressure. These results also suggest that PKC inhibition may have a beneficial role in vascular hyporesponsiveness induced by LPS. Although our study partly elaborated on the effects of LPS on isolated renal vascular responses to vasoactive agents, further studies are required to explain how LPS exerts its renal vascular effects.

Objective(s): Escherichia coli is the key pathogen in the family producing ESBL (extended spectrum β-lactamase) and associated with community-acquired infections. Therefore, this study was planned to determine the antibiotic susceptibility pattern of uropathogenic E. coli, prevalence of the ESBL gene group and class 1 integrons. Materials and Methods: Clinical isolates of uropathogenic E. coli were isolated from different hospitals of Karachi. Antibiotic susceptibility test was performed by Kirby-Bauer Methods. Presence of β – lactamases genes (CTX, TEM, and SHV) and integron 1 were identified by polymerase chain reaction (PCR). Results: Out of 500, 105 isolates were identified as multi-drug resistant (MDR) uropathogenic E. coli. The subject MDR isolates showed the highest resistance to aztreonam, amoxil/ clavulanic acid, ampicillin, cotrimoxazole, ceftriaxone, cefipime, and cefuroxime. Genetic analysis showed that the majority of the MDR E. coli carry CTX M1 (57. 1%) followed by TEM (33. 3%) and SHV (9. 5%). Moreover, 79% of MDR E. coli harbored class 1 integrons, whereas all three conserved genes for class 1 integrons were present in 58% of MDR E. coli. Conclusion: This study is helpful to provide information regarding the antibiotic susceptibility pattern, distribution ESBLs and class 1 integrons among uropathogenic E. coli.

Objective(s): The present study was aimed to evaluate the effect of methanolic fruit extract of Momordica cymbalaria (MeMC) against high-fat diet-induced obesity and diabetes in C57BL/6 mice. Materials and Methods: In the present study, six weeks old male C57BL/6 mice were divided into four groups. G-1 and G-2 served as lean control and HFD control, G-3 and G-4 received MeMC 25 and 50 mg/ kg, BW doses; all the treatments were given for a period of 11 weeks. The parameters such as body weight, fasting blood glucose, insulin, cholesterol, free fatty acid, and oral glucose tolerance tests were performed, further, at the end of the study fasting body weight, and weights of organs such as the liver, heart, and adipose tissue were measured and the liver tissue was subjected to histopathology evaluation, and insulin resistance was expressed as HOMA-IR index. Results: The high-fat diet fed C57 mice showed significant elevation of body weight (P<0. 01), blood glucose (P<0. 01), insulin (P<0. 01), cholesterol (P<0. 01), free fatty acid (P<0. 01), and HOMA-IR index (P<0. 01) along with significant elevation of all organ weights and reduction in oral glucose tolerance (P<0. 01) and brown adipose weight (P<0. 01). The histopathology showed significant fatty infiltration and hypertrophy of hepatocytes. Interestingly, MeMC (50 mg/kg) alleviated all the HFD-induced perturbances significantly. Further, the HPLC analysis of MeMC revealed the presence of gallic acid and rutin as chief ingredients. Conclusion: MeMC possesses potent antidiabetic activity and ameliorates insulin resistance in HFD diet fed C57 mice.