Physiology and Pharmacology
Volume:24 Issue: 2, Jun 2020

Moringa olifera (MO) belongs to Moringaceae family commonly known as the Miracle Tree. It is a versatile tree useful for human beings and animals and also has industrial values. It is one among the richest plant sources of vitamins A, B, C, D, E and K. MO leaves and fruits are used as vegetables in various countries of the world. Earlier studies have found that MO to be nontoxic and recommended for therapeutic use in developing countries. It has been used in treatment of many diseases such as antimicrobial activity, antidiabetic, hepatoprotective, hypo cholesterolemic activity, cancer, high blood pressure and for cardiac stimulation. It is an antioxidant which is known to be more powerful and a free radical scavenger able to inhibit oxidant and stimulate antioxidant status.

The aim of the present study was to evaluate the extent of contribution of thermal regulators in cold stress. Hypothermia is described as a diminution in core body temperature below 35°C. Thermoregulation is the equilibrium between heat generation (thermogenesis) and heat loss (thermolysis). Thermoregulatory control of skin blood flow (SBF) is critical to preserve body temperature homeostasis during thermal changes. The obtained results from different studies revealed that following cold exposure, some areas of the brain like preoptic/anterior hypothalamus, known as body thermostat, involve in thermoregulation by affecting on SBF. Furthermore, some peripheral factors participate in the thermal control through alteration of skin blood flow. Sympathetic neural control of SBF includes the noradrenergic vasoconstrictor system and a sympathetic active vasodilator system. Overall, further future studies are required to elucidate the imbalance of these regulators in some disorders.

The major secondary complications of spinal cord injury (SCI) are neuropathic pain and motor dysfunction, which remained medical challenges for clinicians. Due to the major role of glutamate in excitotoxicity and central sensitization, the present experiment was to evaluate the effects of ketamine (KET), an n-methyl-D-aspartate (NMDA) receptor blocker, on sensory-motor functions in a rat model of clip compression SCI.

Wistar rats were divided into sham, SCI and KET-treated groups. The sham group received laminectomy without any compression lesion. KET and SCI groups were subjected to severe compression injury for 1min with an aneurysm clip and then treated with KET (10mg/kg) or 5% dimethyl sulfoxide (as vehicle), respectively. The rats were assessed by pain-related and motor behavioral tests inclusive of von Frey, acetone drop, hot plate, inclined plane and Basso-Beattie-Bresnahan on day 0 prior to the injury and the 7th, 14th, 21st and 28th days following SCI.

KET group compared with the SCI group showed a significant decline in the mechanical allodynia on the 21st and 28th days, and in cold allodynia from the 1st week to the 4th week post-injury. KET treatment improved the motor function but not weight loss and auricle temperature rise during the 4 weeks of follow up from the 1st week until the 4th week.

It was ultimately attained that the advantageous effects of intrathecal KET on sensory-motor dysfunction of SCI rats could provide new approaches for KET as a neuroprotective agent toward clinical applications.

Cystatin C (CysC) is an indicator of renal function, and has been recently reported that associates with neurodegenerative diseases. To investigate the role of this substance in Parkinson's disease (PD), we evaluated the association between serum levels of CysC and other markers of renal function with 6-hydroxydopamine (6-OHDA) induced Parkinsonism in rat.

The 6-OHDA was microinjected into the medial forebrain bundle by stereotaxic surgery. After behavioral tests, immunofluorescence and biochemical studies were carried out to determine the number of survived dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc) and striatal dopamine level. The blood samples were collected from the caudal vain and the heart of animals. CysC was measured using the enzyme-linked immunosorbent assay (ELISA) kits.

There was no difference in serum level of CysC between the 6-OHDA treated and control groups, as well as before and after the toxin in the 6-OHDA group. Also, no association was found between CysC and DA neuronal death in SNc or striatal dopamine level. In addition, there was no significant difference in serum levels of creatinine, urea and potassium ions between the control and 6-OHDA treated groups.

Since the death of DA neurons in SNc is the main pathophysiological mechanism underlying in the development of both 6-OHDA induced Parkinsonism and PD in human being, CysC and other markers of renal function cannot reflect DA neuronal death and accordingly cannot use for early diagnosis of PD.

Chronic stress impairs memory and certain brain functions such as locomotor activity. Crocin is one of the active components of saffron and has neuroprotective effects on brain functions. This study investigated crocin effects on locomotor activity and recognition of new conditions (exploration time) as well as novel object recognition and object location memories in chronic restraint stress rats.

Thirty-two male Wistar rats were randomly allocated to control group, restraint stress group (6h/day for 21days) and two groups receiving daily intraperitoneal injections of crocin (30 and 60mg/kg) accompanied by restraint stress. Memories were evaluated using the relevant novel object recognition (NOR) and object location (OLT) tests.

The NOR and OLT results, respectively, revealed significant and non-significant decreases in locomotor activity in the stressed group. The NOR results revealed enhanced locomotor activity due to crocin administration (30 and 60mg/kg). The NOR revealed significant enhancements in recognizing new conditions in both crocin treatments while the OLT test did so only with a crocin dose of 60mg/kg. Restraint stress and crocin treatments led to no significant differences in novel object recognition and object location memories. Finally, the stressed group exhibited significant increases in serum corticosterone levels but corticosterone levels declined significantly with crocin dose of 30mg/kg.

The high and low doses of crocin had different effects on the NOR and OLT variables under restraint stress conditions. The NOR test as cognitive test was found more sensitive to crocin treatments than the OLT test as spatial test although neither the memories showed changes in response to such treatment.

Considering the limitations of conventional therapeutic methods in renal failure, researchers are paying attention to the application of adipose-derived mesenchymal stem cells (AD-MSCs) and their protective effects against acute renal failure. This study aims to assess the therapeutic effects of AD-MSCs in gentamicin-induced renal failure in rats.

In this study, 40 male Wistar rats were studied in control, sham, gentamicin treated with and without receiving AD-MSCs. After 10 days, blood samples were collected and hemodynamic parameters, malondialdehyde and ferric reducing antioxidant power (FRAP) measured in the right and left kidneys underwent histologic examination.

Gentamicin administration significantly increased plasma creatinine, blood urea nitrogen, oxidative stress parameters and histologic damages; while significantly reduced FRAP in the gentamicin-receiving group in comparison with the sham group. AD-MSCs treatment significantly improved renal function parameters, oxidative stress and histologic damages in comparison with the gentamicin receiving group.

Intravenous injection of AD-MSCs in gentamicin-induced renal failure improved renal function, oxidative stress parameters and histologic damages.

Considering the cardioprotective and anti-inflammatory properties of statins, the aim of the present experiment was to investigate the possible involvement of inflammatory cytokines in anti-arrhythmic effects of rosuvastatin in both in vitro and in vivo experiments in rats.

Three weeks after oral administration of either of rosuvastatin or vehicle, the atria were removed and after incubation with ouabain, time of onset of arrhythmia and asystole were recorded. We also used immunohistochemistry technique to identify the differentially expressed proteins interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α in atria.

Rosuvastatin significantly postponed the onset of arrhythmia compared to vehicle-treated group. Injection of ouabain increased the atrial expression of IL-1β, IL-6 and TNF-α proteins, while pretreatment of rats with rosuvastatin could significantly attenuate them.

Our data suggest that rosuvastatin exerts anti-arrhythmic properties at least in part through modulation of inflammatory cytokines.

Recently, the therapeutic and antioxidant effects of simvastatin on 7,12-dimethylbenz[a] anthracene (DMBA) induced breast cancer have been studied. To gain further understanding of the molecular mechanisms of simvastatin, this study investigated its effects on the expression of c-myc, cyclin D1 and p53 in normal mammary glands and tumors.

Female albino mice were divided into two groups: 1) N group, healthy mice without DMBA and 2) D group, mice with DMBA administration. After the appearance of tumors, D group mice are subdivided into 3 groups, as control (C), simvastatin- treated group (S) which received 80 mg/kg/day, orally and tamoxifen-treated group (T) with 50 mg/kg/day, orally. After 4 weeks, animals were sacrificed. Also, the tumors and normal mammary glands were removed for histopathological evaluations and analysis of gene expression by qRT-PCR.

The results showed the up-regulation of c-myc and cyclin D1 in tumors of the control group compared with mammary glands of the N group. Similar to tamoxifen, the simvastatin treatment could normalize the expression of c-myc and cyclin D1; however, the expression of p53 did not change in the treated groups.

Down-regulation of c-myc and cyclin D1 in treated tumors with simvastatin could be a possible molecular mechanism for its therapeutic effects in DMBA-induced breast cancer in mice.