Stronger expression of CHOP and caspase 12 in diabetic spinal cord injury rats

Wan, Shuanglin; Shi, Peihua; Zhang, Xiaoming; Gu, Chuanlong; Fan, Shunwu

doi:10.1179/174313209x385707

Cited by 13 publications

(14 citation statements)

References 30 publications

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“…ER stress-induced cell death has been shown to involve the activation of caspase-12, which subsequently activates executer caspases such as caspase-3 [20, 21, 48, 49]. Caspase-12 is specific to insults that elicit ER stress and is not proteolytically activated by other death stimuli [20].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, RQKL also decreased caspase-3 level significantly. Caspase-3 activation is involved in caspase-12 mediated apoptotic cascade, while activated caspase-3 is directly responsible for DNA fragmentation [20, 21, 48]. It is possible that caspase-3 activation is inhibited by suppression of caspase-12.…”

Section: Discussionmentioning

confidence: 99%

“…However, if ER stress is too severe, the unfolded protein response ultimately initiates an apoptotic pathway [19]. ER stress-induced cell death has been shown to involve the activation of caspase-12 [20, 21], while another component of the ER stress-mediated apoptotic pathway is elf-2a [22]. Several studies have shown that cerebral ischemia is a pathological ER stressor, which can trigger the shutdown of protein translation and apoptosis, suggesting that ER plays an important role in cerebral ischemia [23, 24].…”

Section: Introductionmentioning

confidence: 99%

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Refined Qingkailing Protects MCAO Mice from Endoplasmic Reticulum Stress-Induced Apoptosis with a Broad Time Window

Cheng

Zhong

Lü

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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In the current study, we are investigating effect of refined QKL on ischemia-reperfusion-induced brain injury in mice. Methods. Mice were employed to induce ischemia-reperfusion injury of brain by middle cerebral artery occlusion (MCAO). RQKL solution was administered with different doses (0, 1.5, 3, and 6 mL/kg body weight) at the same time of onset of ischemia, and with the dose of 1.5 mL/kg at different time points (0, 1.5, 3, 6, and 9 h after MCAO). Neurological function and brain infarction were examined and cell apoptosis and ROS at prefrontal cortex were evaluated 24 h after MCAO, and western blot and intracellular calcium were also researched, respectively. Results. RQKL of all doses can improve neurological function and decrease brain infarction, and it performed significant effect in 0, 1.5, 3, and 6 h groups. Moreover, RQKL was able to reduce apoptotic process by reduction of caspase-3 expression, or restraint of eIF2a phosphorylation and caspase-12 activation. It was also able to reduce ROS and modulate intracellular calcium in the brain. Conclusion. RQKL can prevent ischemic-induced brain injury with a time window of 6 h, and its mechanism might be related to suppress ER stress-mediated apoptotic signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Refined Qingkailing Protects MCAO Mice from Endoplasmic Reticulum Stress-Induced Apoptosis with a Broad Time Window

Cheng

Zhong

Lü

et al. 2012

Evidence-Based Complementary and Alternative Medicine

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“…Furthermore, activation of the unfolded protein response (UPR) upregulates the expression and activity of caspase-12 and may be important in neuronal cell death in ischemic brain injury (9). It has also been observed that the activation of caspase-12 is involved in the apoptosis of spinal cord neurons and oligodendrocytes, which is induced by oxygen-glucose-serum deprivation/restoration (10,11). Therefore, the inhibition of caspase-12 expression following SCI may potentially be used as a therapeutic target for neuron protection.…”

Section: Introductionmentioning

confidence: 99%

Bone marrow stromal cells inhibit caspase-12 expression in rats with spinal cord injury

Liu¹,

Ding²,

Zhang³

et al. 2013

Experimental and Therapeutic Medicine

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The mechanisms underlying the potentially beneficial effect of bone marrow stem cells (BMSCs) on spinal cord injury (SCI) are unknown. Therefore, the aim of the present study was to explore the protective effect of BMSCs in rats with SCI. A total of 45 adult male Sprague-Dawley rats were randomly divided into three groups; the SCI group (n=15), the BMSC group (n=15) and the sham-operation group (n=15). In the SCI and BMSC treatment groups, a modified Allen’s weight-drop technique was used to induce SCI. The BMSC treatment group received an injection of BMSCs using a microneedle into the epicenter of the spinal cord 24 h after injury. Rats in the sham-operation group were not subjected to SCI; however, the corresponding vertebral laminae were removed. Seven days after transplantation, a rapid recovery was observed in the Basso, Beattie and Bresnahan (BBB) scores of the BMSC treatment group, whereas the BBB scores in the SCI group remained low (P<0.05). Caspase-12 expression in the SCI group was increased compared with that in the sham-operation group, whereas caspase-12 expression was attenuated 24 h after transplantation in the BMSC treatment group (P<0.05). In conclusion, the transplantation of BMSCs may improve locomotor function and attenuate caspase-12 expression following SCI. Therefore, it is likely to be an effective strategy for preventing severe injury of the spinal cord.

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“…8) As a pre-apoptotic factor, CHOP is suggested to activate caspase cascade by inducing cleavage of caspase-12 (rodents) 9) or caspase-4 (human). 10) In recent decades, natural products gradually become new alternatives besides regular therapies. With a long history in traditional medicine in East Asia, ginseng (Panax quinquefolius) is now a very popular herb as medicine or food supplement in the world.…”

mentioning

confidence: 99%

Ginsenoside Rh2 Inhibited Proliferation by Inducing ROS Mediated ER Stress Dependent Apoptosis in Lung Cancer Cells

Gao

Yan

Cai

2017

Biological & Pharmaceutical Bulletin

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Key words ginsenoside Rh2; lung cancer; apoptosis; reactive oxygen species; endoplasmic reticulum stress Followed by serial biological steps including hyperplasia, metaplasia, dysplasia and in situ carcinoma, similar to other cancers, lung cancer eventually develops its malignancy marked by strong proliferative capacity which is characterized by resistance to apoptosis. 1) Nowadays, lung cancer is still among the top common cancers worldwide. According to the records, lung cancer composes 12.7% of cancer and 18.2% of cancer related death.2) Though the multiple therapies including surgery, radiotherapy and chemotherapy are more and more widely applied to patients, the prognosis of lung cancer is still poor due to its malignant nature. Non-small cell lung cancer (NSCLC) takes approximately 85% of lung cancer cases with less than 20% 5-year survival rate.3) Seeking and identifying new drugs inducing apoptosis may provide us new insight into prevention and treatment of lung cancer.As one of the vital organelles in eukaryotic cells, endoplasmic reticulum (ER) is responsible for directing correct protein folding, calcium homeostasis and lipid metabolism. 4) However, under certain physiological and pathological conditions, the normal functions of ER were impaired by multiple extra-or intra-cellular stimuli, which is referred as ER stress.5) Reactive oxygen species (ROS) is considered as one of the stimuli inducing ER stress. This phenotype is called ROS-mediated ER stress. 6) Many anticancer agents such as chemotherapeutic drugs are believed to induce apoptosis by generating excessive intracellular ROS which is related with unfolded protein response (UPR) in ER to induce ER stress. 7) Numerous investigations supposed that ROS-mediated ER stress could further promote cell apoptosis by activating CCAAT/enhancer binding protein (C/EBP) homologous protein CHOP signaling pathway.8) As a pre-apoptotic factor, CHOP is suggested to activate caspase cascade by inducing cleavage of caspase-12 (rodents) 9) or caspase-4 (human). 10)In recent decades, natural products gradually become new alternatives besides regular therapies. With a long history in traditional medicine in East Asia, ginseng (Panax quinquefolius) is now a very popular herb as medicine or food supplement in the world. 11) Extracted from roots of ginseng, ginsenosides are the main effective components.12) It was suggested in the previous study that among the ginsenosides, ginsenoside Rh2 (G-Rh2, first isolated by Shizuo Odashima 13) ) exhibited various biological and pharmacological activities including anti-inflammation, anti-diabetes and anti-cancer. 14-17)A recent report supposed that G-Rh2 induced colorectal cancer cell apoptosis by inducing excessive intracellular ROS generation.18) Thus, ROS-mediated ER-stress induced apoptosis attracted our attention in investigating gensenoside Rh2's mechanism of anti-proliferation.In this present study, we showed G-Rh2 inhibited proliferation of lung cancer cells by inducing apoptosis. Furthermore, whether ROS-mediated ER-s...

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Stronger expression of CHOP and caspase 12 in diabetic spinal cord injury rats

Abstract: These results suggest that stronger ER stress in diabetic rats may be the reason for severe SCI observed.

Cited by 13 publications

References 30 publications

Refined Qingkailing Protects MCAO Mice from Endoplasmic Reticulum Stress-Induced Apoptosis with a Broad Time Window

Refined Qingkailing Protects MCAO Mice from Endoplasmic Reticulum Stress-Induced Apoptosis with a Broad Time Window

Bone marrow stromal cells inhibit caspase-12 expression in rats with spinal cord injury

Ginsenoside Rh2 Inhibited Proliferation by Inducing ROS Mediated ER Stress Dependent Apoptosis in Lung Cancer Cells

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