Microbiological Research and Applied Sciences in the North Eastern Region of India

The northeastern part of India (NE India) is an important biodiversity hotspots and is blessed with a huge diversity of flora and fauna along with other natural resources. Being quite distinct in natural features from rest of the country, NE India has its own unique challenges and opportunities. This part of India is geographically isolated from China by Eastern Himalayas, while tropical forests separate this region from Myanmar and Bangladesh. The armed forces deployed in the NE region have to operate in a wide variety of environments ranging from high altitudes, to tropical rain forests, which pose several operational challenges

Zaštitna uloga amlodipina, blokatora kalcijevih kanala, protiv oštećenja mitohondrija kod ishemičnih i reperfuzijskih ozljeda jetre štakora

Ca2+ accumulation and Ca2+ overloading into mitochondria are responsible for the cell abnormality associated with ischemia and reperfusion injury. The present study was aimed to evaluate the efficacy of Ca2+ channel blocker- amlodipine on the mitochondrial Ca2+ accumulation, mitochondrial antioxidant status and mitochondrial respiratory enzymes in ischemic - reperfusion (I/R) induced liver injury. I/R injury induced mitochondrial damage in rats was assessed in terms of decrease in activities (p< 0.05) of respiratory marker enzymes (malate dehydrogenase, succinate dehydrogenase and NADH –dehydrogenase), mitochondrial antioxidant enzymes (glutathione, superoxide dismutase, catalase), level of lipid peroxidation.(LPO), and Ca2+ accumulation were assessed as marker of mitochondrial damage. Mitochondrial damage was confirmed by transmission electron microscopic (TEM) examination. Pretreatment with amlodipine effectively counteracted the alternation in mitochondrial enzymes induced by ischemia-reperfusion liver damage. TEM study confirms the restoration of cellular normalcy and accredits the cytoprotective role of amlodipine against I/R induced hepatic injury. On the basis of our findings it may be concluded that amlodipine not only possesses Ca2+ channel antagonist properties but it may also reduce the extent of mitochondrial damage by its antioxidant activity.Akumulacija Ca2+ iona i njihovo nakupljanje u mitohondrijima uzrok je abnormalnosti u stanicama nakon ishemičnih i reperfuzijskih ozljeda. Cilj ovog rada bio je ispitati učinak amlodipina, blokatora kalcijevih kanala, na nakupljanje iona kalcija u mitohondrijima, antioksidativni status mitohondrija i na aktivnost enzima u dišnom lancu kod ishemičnih i reperfuzijskih (I/R) ozljeda jetre. Kod tih ozljeda smanjeno je djelovanje (p < 0,05) enzima dišnog lanca (malat dehidrogenaze, sukcinat dehidrogenaze i NADH-dehidrogenaze), antioksidativnih enzima mitohondrija (glutation, superoksid dismutaze, katalaze), stupanj lipidne peroksidacije (LPO) i nakupljanje iona Ca2+. Oštećenje mitohondrija potvrđeno je transmisijskom elektronskom mikroskopijom (TEM). Prethodna obrada s amlodipinom učinkovito sprječava promjenu aktivnosti enzima mitohondrija uzrokovanih I/R oštećenjima jetre. TEM potvrđuje uspostavljanje normalnih uvjeta u stanici i citoprotektivno djelovanje amlodipina. Na temelju rezultata naših istraživanja može se zaključiti da amlodipin zbog antioksidativnog djelovanja reducira oštećenje mitohondrija

Protective effects of amlodipine on mitochondrial injury in ischemic reperfused rat heart Author Details

Abstract The most significant finding of the present study was the release of nitric oxide (NO). The effect of amlodipine on NO production associated with ischemic reperfused (IR) injury was investigated in rat heart model. Cardiac tissues from animal groups were processed for biochemical, histopathological and electron microscopic studies. There was a significant increase in myocardial catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH) enzymes in amlodipine treated group (1.37, 10.27, 6.39) when compared to IR injured group (0.81, 6.87, 4.53). Histopathology studies showed amlodipine reduce cardiocyte damage in cardiac injury during the cardiac IR. Transmission electron microscopic (TEM) study confirmed the cardioprotective role of amlodipine against IR induced cardiac injury. On the basis of findings, it is hypothesized that a portion of the beneficial actions of amlodipine may involve the release or action of NO and probably by its antioxidant properties

Development and Standardisation of a Method for Inflicting Frostbite Injury in Rats and Formulation of Essential Oil in Treatment of Frostbite

Frostbite is a cold induced injury which occurs due to exposure of a particular site of body to sub-zero temperature. One of the primary reasons for lack of proper studies about the underlying mechanism of frostbite injury is due to non-availability of any reliable animal model and method for inflicting frostbite. In our current research, a device was designed and standardised to inflict frostbite wound in wistar rat. A formulation comprising different combination of essential oils was also developed and its activity was assessed and found effective in the treatment of frostbite wound

A small insulinomimetic molecule also improves insulin sensitivity in diabetic mice

Dramatic increase of diabetes over the globe is in tandem with the increase in insulin requirement. This is because destruction and dysfunction of pancreatic β-cells are of common occurrence in both Type1 diabetes and Type2 diabetes, and insulin injection becomes a compulsion. Because of several problems associated with insulin injection, orally active insulin mimetic compounds would be ideal substitute. Here we report a small molecule, a peroxyvanadate compound i.e. DmpzH[VO(O2)2(dmpz)], henceforth referred as dmp, which specifically binds to insulin receptor with considerable affinity (KD-1.17&#x03BC;M) thus activating insulin receptor tyrosine kinase and its downstream signaling molecules resulting increased uptake of [14C] 2 Deoxy-glucose. Oral administration of dmp to streptozotocin treated BALB/c mice lowers blood glucose level and markedly stimulates glucose and fatty acid uptake by skeletal muscle and adipose tissue respectively. In db/db mice, it greatly improves insulin sensitivity through excess expression of PPAR&#x03B3; and its target genes i.e. adiponectin, CD36 and aP2. Study on the underlying mechanism demonstrated that excess expression of Wnt3a decreased PPAR&#x03B3; whereas dmp suppression of Wnt3a gene increased PPAR&#x03B3; expression which subsequently augmented adiponectin. Increased production of adiponectin in db/db mice due to dmp effected lowering of circulatory TG and FFA levels, activates AMPK in skeletal muscle and this stimulates mitochondrial biogenesis and bioenergetics. Decrease of lipid load along with increased mitochondrial activity greatly improves energy homeostasis which has been found to be correlated with the increased insulin sensitivity. The results obtained with dmp, therefore, strongly indicate that dmp could be a potential candidate for insulin replacement therapy

Preparation of Mucoadhesive Patches for Buccal Administration of Metoprolol Succinate: In Vitro and In Vivo Drug Release and Bioadhesion

Purpose: To develop mucoadhesive patches for buccal administration of metoprolol succinate and to evaluate their in vitro and in vivo bioadhesion. Methods: The mucoadhesive buccal patches were prepared by solvent casting technique using two different mucoadhesive polymers. The formulations were tested for in vitro drug permeation studies, buccal absorption, in vitro drug release studies, moisture absorption as well as for in vitro and in vivo bioadhesion. Results: The peak detachment force and work of adhesion for MC5 (sodium carboxymethylcellulose, i.e., Na CMC) patch were 0.87 N and 0.451 mJ respectively and the corresponding values for CH5 (chitosan) were 5.15N and 0.987 mJ. Formulation CH5 (prepared with chitosan) showed 67.1 % release, while MC5 (Na CMC) showed drug release of 81.9 % in 6 h. Basic pharmacokinetic parameters such as Cmax, Tmax and AUCtotal varied statistically (p<0.05) when given by the buccal route compared with that of the solution given by the oral route. Conclusion: The results indicate that formulation of suitable bioadhesive buccal patches with the desired permeability is feasible. The development of bioadhesive buccal formulation for metoprolol succinate with a lower dose and few side effects may be attainable

Protective effect of L-arginine against necrosis and apoptosis induced by experimental ischemic and reperfusion in rat liver

BACKGROUND/AIM: To study the effect of L-arginine on apoptosis and necrosis induced by 1-h ischemia followed by 3-h reperfusion. MATERIALS AND METHODS: Adult Wistar rats underwent 60 min of partial liver ischemia followed by 3-h reperfusion. Eighteen Wistar rats were divided into sham-operated control group (I) (n = 6), ischemia and reperfusion (I/R) group (0.9% saline (5 mL/kg, orally) for 7 days) (II) (n = 6), and L-arginine-treated group (10 mg/kg body weight daily orally for 7 days before inducing ischemia-reperfusion maneuver) (III) (n = 6). Apoptotic and necrotic hepatocytes, nitric oxide levels in hepatocytes, Bcl-2 mRNA, and Bcl-2 protein were measured. Liver injury was assessed by plasma alanine transaminases (ALT), aspartate transaminases (AST), liver histopathology, and electron microscopy. RESULTS: An ischemic and reperfusion hepatocellular injury occurred as was indicated by increased serum ALT, AST, histopathology, and electron microscopy. Apoptosis and necrosis associated marker gene Bcl-2 mRNA and protein expression were decreased in I/R group. Pretreatment with L-arginine significantly decreased serum ALT and AST level and apoptotic and necrotic cells after 1 h ischemia followed by 3 h of reperfusion. Nitric oxide production in hepatocytes was increased twofold by L-arginine treatment when compared with I/R group. Histopathology and transmission electron microscopy (TEM) studies showed markedly diminished hepatocellular injury in L-arginine-pretreated rats during the hepatic I/R. CONCLUSION: Thus, it may be concluded that L-arginine afforded significant protection from necrosis and apoptosis in I/R injury by upregulated Bcl-2 gene and nitric oxide production

Effects of Calendula Essential Oil-Based Cream on Biochemical Parameters of Skin of Albino Rats against Ultraviolet B Radiation

Reactive oxygen species (ROS) generated from UV-B radiation have the capacity to cause oxidative decomposition which leads to the formation of toxic components as well as lipid peroxidation. Considering this fact, the present study was performed to evaluate the effect of a cream (O/W) containing the essential oil of Calendula officinalis on biochemical parameters of the skin of albino rats against UV-B radiation. The fingerprint analysis of Calendula essential oil was performed by HPLC with special reference to 1,8-cineole and α-pinene. The results indicated that the treatment with creams containing 4% and 5% of Calendula essential oil caused a significant decrease in the malonyldialdehyde level, whereas the levels of catalase, glutathione, superoxide dismutase, ascorbic acid, and the total protein level were significantly increased after 1 month of daily irradiation and treatment when compared to untreated control groups. The results suggest that the cutaneous application of the essential oil of Calendula prevents UV-B-induced alterations in the level of antioxidants in skin tissue