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Introduction: Diabetic neuropathy is a common complication of diabetes mellitus. It is associated with nerve damage due to oxidative stress and high levels of pro-inflammatory mediators. In the present study, we examined the anti-nociceptive effects of Fullerene nanoparticle, as a potent anti-oxidant, during diabetic neuropathy. Methods: Diabetes mellitus induced through injection of streptozotocin (STZ) (40 mg/kg). Four groups were used in the study as follows: the control, control+fullerene, diabetes, and diabetes +fullerene groups. All four groups received sesame oil. Treatment rats received fullerene C60 (1mg/kg/day) for 9 weeks by intra-gastric gavage. Then, cold allodynia, histology, and tumor necrosis factor-α (TNF- α) protein expression of the hippocampus were measured 9 weeks after injection of STZ. Results: Our data revealed that STZ induces cold allodynia in both hind paws and increases the TNF- α protein expression in the hippocampus. Furthermore, STZ induces neural degeneration in the hippocampus. Additionally, fullerene C60 significantly attenuated cold allodynia and TNF- α protein expression. Also, fullerene C60 has neuro-protective effects on hippocampal neurons. However, fullerene C60 did not significantly reduce serum glucose levels in diabetic animals. Conclusion: Our data suggest that fullerene C60 likely suppressed pain, and neural loss by inhibitory effects on TNF- α protein expression in the hippocampus during diabetes. [ABSTRACT FROM AUTHOR]

Resveratrol as a natural polyphenolic agent can alleviate neuropathic pain symptoms. The mechanism of analgesic activity of resveratrol is far from clear. The current study examine whether analgesic activity of resveratrol is mediated by its neuroprotective and anti-oxidant activity in the neuropathic pain. We further examine whether analgesic activity of resveratrol is mediated by β-adrenoceptors in the brain. Neuropathic pain induced by L5 spinal nerve ligation (SNL). Male Wistar rats assigned into sham, SNL, SNL + resveratrol (40 μg/5 μL), and SNL + resveratrol + propranolol (a non-selective β-adrenoceptor antagonist, 30 μg/5 μL) groups. Drugs injected intracerebroventricular (ICV) at day SNL surgery and daily for 6 days following SNL. Thermal allodynia and anxiety examined on days of −1, 2, 4, and 6 following SNL. Electrophysiological study performed on day 6 following SNL for evaluation of resveratrol effects on sciatic nerve conduction velocity (NCV). The activity of catalase (Cat) and superoxide dismutase (SOD) enzymes in the brain assessed on days 6 following SNL. Resveratrol significantly decreased thermal allodynia (and not anxiety) in all experimental days. Additionally, resveratrol significantly increased NCV, and also normalized the disrupted Cat and SOD activities following neuropathic pain. Furthermore, propranolol significantly blocked the analgesic and neuroprotective effects of resveratrol. It is suggested that the analgesic effects of resveratrol is mediated by its neuroprotective and antioxidant activities in the neuropathic rats. Furthermore, propranolol blocked the analgesic and neuroprotective effects of resveratrol. [ABSTRACT FROM AUTHOR]

Background and Objectives: Nosocomial infections (NIs) are an important cause of mortality and morbidity in intensive care units (ICU). Pneumonia is the most common serious manifestation of infection in Covid-19 patients. The aim of this study was to investigate the prevalence of pneumonia in Covid-19 patients admitted to the ICU. Materials and Methods: In this cross-sectional study, 1240 Covid-19 patients admitted for more than 48 h in the ICUs of Imam Khomeini Complex Hospital (IKCH) in Tehran for seven months in 2020 were included in the study with initial diagnosis of Covid-19 (PCR test and chest imaging). Data were collected regarding severity of the illness, primary reason for ICU admission, presence of risk factors, presence of infection, length of ICU and hospital stay, microbial type and antibiotic resistance. In this study, the pattern of antibiotic resistance was determined using the disk difusion method. Results: In this study, 289 (23.3%) out of 1320 patients experienced NIs. 221 (76.4%) out of 289 patients had underlying diseases and the most common of which were hypertension, diabetes and heart disease, respectively. 163 patients (56.4%) were RT-PCR COVID-19 positive and 200 patients (69%) died. The majority of patients with NIs (71%) were over 55 years old. The most common type of nosocomial infection (66%) was ventilator-associated pneumonia (VAE). The most common microorganisms that cause pneumonia were Acinetobacter baumannii, Klebsiella pneumoniae and Pseudomonas aeruginosa, respectively. Conclusion: Pneumonia infection is high in Covid-19 patients admitted to the ICU, it needs to be planned with the diagnosis and measures related to the control and prevention of this infection. [ABSTRACT FROM AUTHOR]

Objective: Oxidative stress in diabetic mellitus is a consequence of oxidative stress, which plays a critical role in the pathogenesis of diabetic tissue damage. Receptors for advanced glycation end products and for oxidized low-density lipoproteins (LDL) have critical contribution in oxidative tissue damage. The present study investigated whether anti-diabetic effects of Crocin via modulation of mRNA expression of RAGE and LOX-1 receptors in diabetic rats. Methods: In the current study, high-fat cholesterol (HFC) and streptozotocin (40 mg/kg) used to induce type II diabetes. Experimental groups as follows: (Group 1: control); (Group 2: control treatment [Crocin]); (Group 3: DM [STZ]); (Group 4: DM treatment [STZ + Crocin]); (Group 5; DM + HFC [STZ + HFC]); (Group 6; DM + HFC treatment [STZ + HFC + Crocin]). Crocin (20 mg/kg/day, i.p.) administered in treatment groups for 60 days. Serum glucose and cholesterol levels evaluated on days 5, 30 and 60 after induction of DM. Pancreatic tissue from all group removed on day 60 for histological and RT-PCR analysis. Results: Application of Crocin significantly decreased serum cholesterol levels on day 60 after induction of DM in diabetic + HFC rats. Moreover, Crocin significantly decreased serum glucose levels on days 30 and 60 both in diabetic and diabetic + HFC rats. Crocin partially prevented the atrophic effects of STZ on both exocrine and endocrine parts of pancreas. Additionally, Crocin significantly decreased LOX-1 and RAGE mRNA expression OF pancreas in diabetic rats. Conclusion: The current study suggested that Crocin suppressed atrophic change of the pancreas by decrease of LOX-1 and RAGE mRNA expression in diabetic rats. [ABSTRACT FROM AUTHOR]

Introduction: According to the powerful antioxidant effects of rosuvastatin, the present study aimed to examine the protective effects of rosuvastatin against oxidative damage of diabetic pancreas by potentiation of the antioxidant capacity in streptozotocin-induced diabetic rats. Methods: Experiment was performed in four groups of male Wistar rats (n=6 in each group): normal, diabetic and two treatment groups (normal and diabetic rats treated with rosuvastatin). Rats were made diabetic by a single intravenous injection of streptozotocin (40 mg/kg) at the beginning of study. Treatment groups received orally rosuvastatin at dose of 10 mg/kg/day. After eight weeks, the pancreas tissues were removed under deep anesthesia. After tissue homogenization, the contents of glutathione and malondialdehyde (MDA) as well as superoxide dismutase (SOD) activity were assessed by biochemical methods. Results: Blood glucose of diabetic rats was above 350 mg/dl. The MDA content of the homogenized pancreas significantly increased in diabetic rats by 92%. Diabetes also decreased the content of glutathione (32%) as well as SOD activity (68%) of pancreas tissues. Treatment with rosuvastatin noticeably decreased the MDA levels of diabetic pancreas (90%). Moreover, rosuvastatin significantly increased the glutathione content (21%) and SOD activity (67%) of pancreas tissues in treated diabetic rats. Conclusion: Our findings reveal that rosuvastatin is able to attenuate the uncontrolled hyperglycemia-induced oxidative damage of pancreas through potentiation of the antioxidant defense system. [ABSTRACT FROM AUTHOR]

Purpose: Previous findings have shown the crucial roles of brain renin-angiotensin system (RAS) in pathogenesis of Alzheimer's disease (AD). Since RAS inhibitors may have beneficial effects on dementia and cognitive function in elderly people, the aim of present study was to examine the neuroprotective actions of captopril and valsartan on memory function and neuronal damage in experimental model of AD. Methods: Adult forty male Wistar rats (220-280g) were randomly divided into 5 groups; Control, Vehicle, Alzheimer and treatment groups. AD was induced by the injections of streptozotocin (3mg/kg, bilateral intracerebroventricular) at days 1&3. Treated rats received orally captopril (50mg/kg/day) and valsartan (30mg/kg/day). Memory function and histological assessments were done at termination of experiment. Finally, superoxide dismutase (SOD) and catalase (CAT) activities as well as malondialdehyde (MDA) and NOx contents were determined. Results: There was a significant increase in the mean value of latency in Alzheimer group (66%). Captopril and valsartan considerably decreased this value in both treatment groups (45% and 72%, respectively). In Alzheimer group the activities of brain's SOD and CAT reduced (40% and 47%, respectively) in accompany with an increase in MDA and NOx contents (49% and 50%, respectively). Captopril and valsartan significantly increased the activities of brain's SOD and CAT concomitant reduction in MDA and NOx contents. Also, histopathological damages noticeably decreased in both treatment groups. Conclusion: Our findings indicate that RAS inhibition by using captopril and valsartan potentiates the antioxidant defense system of brain and reduces oxidative/nitrosative stress in accompany with neuronal damage during AD. [ABSTRACT FROM AUTHOR]

Objective: Atorvastatin has the pleiotropic effects, including antiinflammation and antioxidant. Therefore, this study considered to examine the effects of atorvastatin on NF-κB expression, as a main transcription factor for expression of inflammatory cytokines, in hyperglycemia-induced nephropathy in rat. Materials and Methods: Twenty four male Wistar rats were randomly divided into four groups; Normal, Normal treatment, Diabetic, and Diabetic treatment. Rats were made diabetic by an intravenous injection of streptozotocin (40 mg/kg). Treated rats received atorvastatin for 60 days (40 mg/kg/day). At the end of experiment, blood samples were collected for measurement of blood glucose. Moreover, the mRNA expression level of NF-κB in kidney was determined by RT-PCR technique. Results: Induction of diabetes significantly increased the mean value of blood glucose in diabetic rats (>450 mg/dl) compared with normal rats (P=0.001). Chronic hyperglycemia also increased the mRNA expression level of NF-κB in diabetic kidney. Moreover, the mean value of kidney index was significantly increased in diabetic rats compared to normal group (P=0.001). Treatment with atorvastatin in diabetic rats for 60 days reduced the mRNA expression level of NF-κB and kidney index compared to nontreated diabetic rats (P=0.014). Conclusion: Our findings revealed that atorvastatin is able to prevent the development of diabetic nephropathy during chronic uncontrolled hyperglycemia possibly by the inhibition of NF-κB expression in the kidneys of diabetic rats. [ABSTRACT FROM AUTHOR]

Aminoglycosides are still widely used for treatment of gram-negative sepsis in critically ill patients. The most reported electrolyte abnormalities related to these drugs are hypokalemia, hypomagnesemia, and hypocalcemia. In this study potential benefit of atorvastatin in prevention of amikacin-induced electrolytes imbalances has been evaluated. In this trial 44 patients were assigned to the atorvastatin or placebo group based on the simple randomization method. Atorvastatin group received amikacinwith dose of 15 mg/kg/day in two equal divided doses every 12 h as intravenous infusion during 30 min and atorvastatin 40 mg tablet as daily oral dose for 7 days. Patients in the placebo group received same dose of amikacinand placebo tablet (Placebo group) for at least 7 days. Serum electrolytes (sodium, potassium, calcium, phosphor and magnesium) concentrations, blood urea nitrogen and serum creatinine levels were measured at day 0 and end of the study. Baseline mean ± SDof serum potassium concentration in the atorvastatin and placebo group was 4.07± 0.37 and 4.15 ± 0.53 meq/l respectively (p=0.88). Serum potassium concentration remained unchanged at the end of the study in the atorvastatin group (P=0.61) but significantly decreased from 4.15 ± 0.53 to 3.80 ± 0.55meq/l in the placebo group at day 7(P = 0.02).In this pilot study, atorvastatin as 40 mg daily oral dose prevented renal potassium loss during course of amikacin therapy in the critically ill patients. In the future well designed randomized clinical trials with adequate sample size, renoprotective effects of statins should be examined. [ABSTRACT FROM AUTHOR]