NOPR Collection:http://nopr.niscpr.res.in/handle/123456789/636162026-10-09T20:39:21Z2026-10-09T20:39:21ZMagnesium oxide nanoparticles administered orally promote degenerative changes and dysfunctioning in the brainShaikh, Shamshad MDesai, PVhttp://nopr.niscpr.res.in/handle/123456789/636252024-03-27T05:58:35Z2024-04-01T00:00:00ZTitle: Magnesium oxide nanoparticles administered orally promote degenerative changes and dysfunctioning in the brain
Authors: Shaikh, Shamshad M; Desai, PV
Abstract: Magnesium oxide nanoparticles (MgO NPs) have shown immense potential due to their unique and versatile properties useful for various biological applications. However, concerns about their potential toxicity to living organisms and the environment invite thorough assessment of their safety and long-term effects. Here, we examined the in vivo effects of MgO NPs on the brain in order to assess their potential harm. The result revealed that MgO NPs when administered orally, induced degenerative changes in brain regions like the cerebrum, cerebral cortex, medulla oblongata, and olfactory bulb. A reduction in granular, molecular, Purkinje, glial, and pyramidal cells, as well as degeneration, inflammation, and induction of pyknosis of nuclei in mitral cells and vacuolation in the granular and plexiform layers, are among these alterations. ALP, SGOT, SGPT, AChE, GS, Mg2+- ATPases, Ca+2- ATPases, GPx, SOD, and catalase activities declined by MgO NPs, while those of ACP, GD, and Na+-K+- ATPases activities elevated. Antioxidant concentrations, specifically TBARS, increased while reduced glutathione decreased. Neurotransmitters like glutamate levels were elevated, whereas those of dopamine, serotonin, and GABA declined. As a result, the study provides a glimpse into the adverse effects of MgO NPs, demonstrating their potential risk in medicine and various applications, as the alterations caused by these NPs would not only impede regular brain activity, causing neurological disorders but may also disrupt the entire organ system.
Page(s): 229-2372024-04-01T00:00:00ZRole of cannabinoid CB1 receptors in the proconvulsant effect of Apelin-13 on penicillin-induced epileptiform activityAycik, Fatma BanuAyyildiz, MustafaAgar, Erdalhttp://nopr.niscpr.res.in/handle/123456789/636242024-03-27T05:57:13Z2024-04-01T00:00:00ZTitle: Role of cannabinoid CB1 receptors in the proconvulsant effect of Apelin-13 on penicillin-induced epileptiform activity
Authors: Aycik, Fatma Banu; Ayyildiz, Mustafa; Agar, Erdal
Abstract: Epilepsy is a widespread neurological disorder. Many neurotransmitters, neuropeptides and neuromodulators have a
significant role in the epileptic activity. Apelin-13 and cannabinoid CB1 receptor agonist and antagonist have an effect in
the penicillin model of epilepsy. The relationship between apelin and epilepsy, and the apelin-cannabinoid relationship in
epilepsy is still not well understood. Thus, this study focuses on the relationship between apelin-13 and CB1 receptor in
experimental model of epilepsy. Penicillin injection was given intracortically (i.c.) for the development of epileptic seizures.
Ninety-one male Wistar rats were divided into 13 groups. CB1 receptor agonist ACEA (7.5 μg, intracerebroventricularly,
icv) and antagonist AM-251 (0.25 μg and 0.125 μg, icv) were administered to three different groups, two different doses of
apelin-13 (5 μg and 15 μg, icv) were applied and the interactions between these five groups of substances were evaluated.
Both apelin-13 (15 μg) and AM-251 (0.25 μg) raised the spike frequency of epileptiform activity separately. Application of
apelin-13 + AM-251 also increased the spike frequency of epileptiform activity beginning in the 30 min after apelin-13
application. When the non-effective dose of AM-251 and the effective dose of apelin-13 were administered together,
epileptic activity increased in the 20 min. ACEA reduced the epileptiform activity starting in the 50th min. apelin-13 and
ACEA administration in effective doses decreased epileptiform activity. The non-effective doses of AM-251, apelin-13 and
effective dose of ACEA decreased the epileptiform activity in the 50 min. Application of non-effective doses of apelin and
AM-251 together does not induce any additional proconvulsant activity, and CB1 receptor agonist, ACEA reversed the
proconvulsant activity of apelin-13. These results suggest that they utilize different receptors to begin their own effects by
increasing intracellular Ca2+ in epilepsy. Considering that apelin-13 is an endogenous substance known for its
neuroprotective properties, the proconvulsant effect of apelin-13 in the presented study is remarkable.
Page(s): 238-2442024-04-01T00:00:00ZWithania somnifera (L.) Dunal ameliorates imidacloprid induced neurotoxicity: Inhibition of oxidative stress, apoptosis and downregulation of glial fibrillary acidic protein in female Wistar ratsSoujanya, SLakshman, MMadhuri, DReddy, A GopalaRao, SV Ramahttp://nopr.niscpr.res.in/handle/123456789/636232024-03-27T05:55:39Z2024-04-01T00:00:00ZTitle: Withania somnifera (L.) Dunal ameliorates imidacloprid induced neurotoxicity: Inhibition of oxidative stress, apoptosis and downregulation of glial fibrillary acidic protein in female Wistar rats
Authors: Soujanya, S; Lakshman, M; Madhuri, D; Reddy, A Gopala; Rao, SV Rama
Abstract: In agricultural farming, neonicotinoid insecticides are used to control insect pests on agricultural crops and ectoparasitic
arthropods on animals. Here, we evaluated the oral toxicity of one of the commonly used neonicotinoid insecticides,
imidacloprid (IMI) on the brain tissue of female Wistar rats and its amelioration by Indian ginseng, Withania somnifera (L.)
Dunal. The study was conducted on a total of 48 female Wistar rats divided into four groups, each containing 12 rats.
Gr. I was normal control; Gr. II, imidacloprid; Gr. III, W. somnifera; and Gr. IV with both imidacloprid and W. somnifera.
The rats were subjected to oral treatment of W. somnifera (1 g/kg feed) for a period of 30 days to measure the protective
effect against neurotoxicity induced by imidacloprid (30 mg/kg body wt./day). Six rats from each group were sacrificed on
16th and 31st day. The results showed that imidacloprid significantly decreased the reduced glutathione, super oxide
dismutase and increased the thio barbituric acid reactive substance (TBARS) levels. It also caused histopathological,
immunohistochemical and ultrastructural changes in the brain. Whereas, W. somnifera significantly increased the reduced
glutathione, super oxide dismutase (SOD) and reduced the TBARS levels. Further, it inhibited apoptosis by upregulation of
B-cell lymphoma 2 protein and reduced the neuronal degeneration by downregulation of glial fibrillary acidic protein. These
results indicate that Withania somnifera may be beneficial in ameliorating the imidacloprid induced oxidative stress and
apoptosis in the brain tissue of rats.
Page(s): 245-2532024-04-01T00:00:00ZDownregulation of HSP27 by isoindole-derived pyrrolidines suppressing multidrug resistance (MDR) and inducing apoptosis in MCF-7 and DLD-1 cell linesMesci, SedaYazgan, BurakGül, MelekYıldırım, Tubahttp://nopr.niscpr.res.in/handle/123456789/636222024-03-27T05:52:40Z2024-04-01T00:00:00ZTitle: Downregulation of HSP27 by isoindole-derived pyrrolidines suppressing multidrug resistance (MDR) and inducing apoptosis in MCF-7 and DLD-1 cell lines
Authors: Mesci, Seda; Yazgan, Burak; Gül, Melek; Yıldırım, Tuba
Abstract: In most cancer treatments, major problem arises from the prevention of cell death (apoptosis suppression) with the development
of drug resistance. Anticancer agents that ensure elimination of drug resistance and drug-resistant cells to apoptosis, are among the
main targets. Here, we evaluated a series of synthesized N-phenyl maleimide substituents in tetracyclic compounds as anticancer
drug candidate. We selected compounds may lead to death and eliminate drug resistance in breast and colon cells. In MCF-7 and
DLD-1 cell lines; multidrug resistance genes (ABCB1, ABCC3, ABCC10, ABCC11 and ABCG2), apoptosis mechanism genes
(BAX, BCL-2, p53, PARP and CASP3), heat shock genes (HSP27, HSP40, HSP60, HSP70 and HSP90α) and endoplasmic
reticulum (ER) chaperone genes (GRP78 and GRP94) mRNA levels were determined by qPCR method. Amounts of proteins of
apoptosis and signalling pathways were measured by human apoptosis antibody array. The compounds have been shown to have
downregulation on multidrug resistance genes other than ABCC3. It was found that all compounds in MCF-7 and DLD-1 cells
showed significant increase in p53, BAX and CASP3 gene expressions. Also, the compounds have the potential to reduce gene
expression of heat shock genes (HSPs). While the compounds have been determined to increase protein expression in BAD,
BAX, BID, BIM, Caspase-3, Caspase-7, Caspase-8, Cytochrome-C, Fas, TNF, TRAIL, p27, p38 and p53; decrease protein
expression in AKT, BCL-2, ERK1/2, HSP27, HSP60, IGFs, JNK, NFKB, PARP, TAK1, Survivin in MCF-7 and DLD-1 cells. The
compounds stand out with their inhibition of HSP27 in DLD-1 cells and their inhibition with HSP27 and NFB in MCF-7 cells.
Overall, it has been shown that these compounds increase intrinsic and extrinsic proapoptotic proteins, decrease antiapoptotic
proteins, decrease HSPs and some growth factors, and they may serve as potential anticarcinogenic molecules.
Page(s): 254-2652024-04-01T00:00:00Z