scholarly journals The Protective Effects of Insulin and Natural Honey against Hippocampal Cell Death in Streptozotocin-Induced Diabetic Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Iraj Jafari Anarkooli ◽  
Hossein Barzegar Ganji ◽  
Maryam Pourheidar
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Living Cells ◽  
Diabetic Rats ◽  
Control Group ◽  
Protective Effects ◽  
Hippocampal Cell ◽  
Group I ◽  
Group D

We investigated the effects of insulin and honey as antioxidants to prevent the hippocampal cell death in streptozotocin-induced diabetic rats. We selected sixty Wister rats (5 groups of 12 animals each), including the control group (C), and four diabetic groups (control (D) and 3 groups treated with insulin (I), honey (H), and insulin plus honey (I + H)). Diabetes was induced by streptozotocin injection (IP, 60 mg/kg). Six weeks after the induction of diabetes, the group I received insulin (3-4 U/kg/day, SC), group H received honey (5 mg/kg/day, IP), and group I + H received a combination of the above at the same dose. Groups C and D received normal saline. Two weeks after treatment, rats were sacrificed and the hippocampus was extracted. Neuronal cell death in the hippocampal region was examined using trypan blue assay, “H & E” staining, and TUNEL assay. Cell viability assessment showed significantly lower number of living cells in group D than in group C. Besides, the mean number of living cells was significantly higher in group I, H, and I + H compared to group D. Therefore, it can be concluded that the treatment of the diabetic rats with insulin, honey, and a combination of insulin and honey can prevent neuronal cell death in different hippocampal areas of the studied samples.

scholarly journals Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat

2016 ◽  
Vol 88 (suppl 1) ◽  
pp. 653-663 ◽  
Author(s):  
Dulce-Mariely Álvarez-Croda ◽  
Juan Santiago-García ◽  
Jesús S. Medel-Matus ◽  
Joel Martínez-Quiroz ◽  
Angel A. Puig-Lagunes ◽  
...  
Keyword(s):  
Cell Death ◽  
Status Epilepticus ◽  
Mrna Expression ◽  
Dorsal Hippocampus ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Control Group ◽  
Rat Pups ◽  
Fluoro Jade B ◽  
Developing Rat

The contribution of Interleukin-1β (IL-1β) to neuronal injury induced by status epilepticus (SE) in the immature brain remains unclear. The goal of this study was to determine the hippocampal expression of IL-1β and its type 1 receptor (IL-1RI) following SE induced by the lithium-pilocarpine model in fourteen-days-old rat pups; control animals were given an equal volume of saline instead of the convulsant. IL-1β and IL-1RI mRNA hippocampal levels were assessed by qRT-PCR 6 and 24 h after SE or control conditions. IL-1β and IL-1RI expression was detected in the dorsal hippocampus by immunohistochemical procedures; Fluoro-Jade B staining was carried out in parallel sections in order to detect neuronal cell death. IL-1β mRNA expression was increased 6 h following SE, but not at 24 h; however IL-1RI mRNA expression was unaffected when comparing with the control group. IL-1β and IL-1RI immunoreactivity was not detected in control animals. IL-1β and IL-1RI were expressed in the CA1 pyramidal layer, the dentate gyrus granular layer and the hilus 6 h after SE, whereas injured cells were detected 24 h following seizures. Early expression of IL-1β and IL-1RI in the hippocampus could be associated with SE-induced neuronal cell death mechanisms in the developing rat.

scholarly journals Protective effects of cyclohexenone long chain alcohols against the neuronal cell death due to calcium overloading

2000 ◽  
Vol 82 ◽  
pp. 178
Author(s):  
Mihoko Hirata ◽  
Remi Tsuchiya ◽  
Miyuki Ogawa ◽  
Nagisa Matsumoto ◽  
Masashi Yamada ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Protective Effects ◽  
Calcium Overloading ◽  
Long Chain

scholarly journals 1-O-Hexyl-2,3,5-Trimethylhydroquinone Ameliorates l-DOPA-Induced Cytotoxicity in PC12 Cells

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 867 ◽  
Author(s):  
Hyun Park ◽  
Jong Kang ◽  
Myung Lee
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Pc12 Cells ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mitogen Activated Protein Kinase ◽  
Protective Effects ◽  
Extracellular Signal ◽  
Dopaminergic Neuronal Cell ◽  
Mitogen Activated Protein

1-O-Hexyl-2,3,5-trimethylhydroquinone (HTHQ) has previously been found to have effective anti-oxidant and anti-lipid-peroxidative activity. We aimed to elucidate whether HTHQ can prevent dopaminergic neuronal cell death by investigating the effect on l-DOPA-induced cytotoxicity in PC12 cells. HTHQ protected from both l-DOPA-induced cell death and superoxide dismutase activity reduction. When assessing the effect of HTHQ on oxidative stress-related signaling pathways, HTHQ inhibited l-DOPA-induced phosphorylation of sustained extracellular signal-regulated kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK1/2). HTHQ also normalized l-DOPA-reduced Bcl-2-associated death protein (Bad) phosphorylation and Bcl-2-associated X protein (Bax) expression, promoting cell survival. Taken together, HTHQ exhibits protective effects against l-DOPA-induced cell death through modulation of the ERK1/2-p38MAPK-JNK1/2-Bad-Bax signaling pathway in PC12 cells. These results suggest that HTHQ may show ameliorative effects against oxidative stress-induced dopaminergic neuronal cell death, although further studies in animal models of Parkinson’s disease are required to confirm this.

Characterization of neuronal cell death in normal and diabetic rats following exprimental focal cerebral ischemia

Life Sciences ◽  
2001 ◽  
Vol 69 (23) ◽  
pp. 2801-2810 ◽  
Author(s):  
Gui-Xia Wang ◽  
Guang-Ren Li ◽  
Ying-Di Wang ◽  
Tong-Shu Yang ◽  
Yi-Bing Ouyang
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Diabetic Rats

Protective effects of a selective L-type voltage-sensitive calcium channel blocker, S-312-d, on neuronal cell death

2004 ◽  
Vol 67 (6) ◽  
pp. 1153-1165 ◽  
Author(s):  
Tatsurou Yagami ◽  
Keiichi Ueda ◽  
Toshiyuki Sakaeda ◽  
Naohiro Itoh ◽  
Gaku Sakaguchi ◽  
...  
Keyword(s):  
Cell Death ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Protective Effects

scholarly journals Protective Effects of Bupivacaine against Kainic Acid-Induced Seizure and Neuronal Cell Death in the Rat Hippocampus

2015 ◽  
Vol 38 (4) ◽  
pp. 522-530 ◽  
Author(s):  
Kuan Ming Chiu ◽  
Chia Chan Wu ◽  
Ming Jiuh Wang ◽  
Ming Yi Lee ◽  
Su Jane Wang
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Hippocampus ◽  
Protective Effects

scholarly journals Protective Effects of Chunghyuldan against ROS-mediated Neuronal Cell Death in Models of Parkinson’s Disease

2010 ◽  
Vol 107 (6) ◽  
pp. 958-964 ◽  
Author(s):  
Hyo Geun Kim ◽  
Mi Sun Ju ◽  
Dong-Hyun Kim ◽  
Jongki Hong ◽  
Seung-Hun Cho ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Protective Effects

scholarly journals Protective Effects of 4-Phenylbutyrate Derivatives on the Neuronal Cell Death and Endoplasmic Reticulum Stress

2012 ◽  
Vol 35 (1) ◽  
pp. 84-90 ◽  
Author(s):  
Seisuke Mimori ◽  
Yasunobu Okuma ◽  
Masayuki Kaneko ◽  
Koichi Kawada ◽  
Toru Hosoi ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Endoplasmic Reticulum Stress ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Protective Effects

scholarly journals The Efficacy of Cinnamomum burmanii Extract on the Protection of Neuronal Cell Death in Haloperidol Induced Male Wistar Rats

2018 ◽  
Vol 2 (4) ◽  
pp. 1-11
Author(s):  
Nita Parisa ◽  
MT Kamaluddin ◽  
Theodorus Theodorus
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Positive Control ◽  
Control Group ◽  
Cinnamon Extract ◽  
White Rats ◽  
Before And After ◽  
Mean Differences

Background Haloperidol is categorized as the first class antipsychotic drug. Long-term use of haloperidol may convey to increased Reactive Oxygen Species (ROS) that will yield oxidative damage which further leads to cell death. Several studies had identified the effects of cinnamon extract on cell death. This study aimed to determine the efficacy of cinnamon extract (Cinnamomum burmanii) on the protection of neuronal cell death in haloperidol-induced male Wistar white rats. Methods This study was experimental with pre and post-test design. Thirty male Wistar rats were divided into 5 groups, induced with haloperidol and followed by treatment. Caspase-3 and dopamine were assayed by ELISA sandwich method using ELISA kit. Mean difference of caspase expression and dopamine levels before and after induction were shown (p<0.05). Results There were mean differences of caspase-3 expression level in the positive control group, cinnamon extract of 100 and 200mg/kgBW before and after treatment (p<0.05). Whereas for dopamine levels, there were mean differences in positive control group, cinnamon extract of 50, 100 and 200mg/kgBW before and after treatment (p<0.05). With Post Hoc test, it was found that there were no mean differences of caspase-3 expression level between positive group with cinnamon extract group of 100 and 200mg/kgBW (p>0,05) and there were also no mean differences of positive group dopamine level with group of cinnamon extract of 100 and 200mg/kgBW (p>0.05). Conclussion Cinnamomum burmanii extract at dose of 100 and 200mg/kgBW were effective in the protection against neuronal cell death in haloperidol induced male Wistar white rats.

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