Ceramide generation during curcumin-induced apoptosis is controlled by crosstalk among Bcl-2, Bcl-xL, caspases and glutathione

Shakor, Abo Bakr Abdel; Atia, Mona; Alshehri, Ali; Sobota, Andrzej; Kwiatkowska, Katarzyna

doi:10.1016/j.cellsig.2015.07.022

Cited by 20 publications

(11 citation statements)

References 64 publications

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“…Parallel to these results, Pan et al, [] reported that ACR triggered the mitochondrial apoptotic pathway in PC12cells and increased up regulation of the Bax/Bcl2 ratio, liberation of cytochrome c, activation of capase‐9 and caspase‐3 and mitochondrial dysfunction. It is noteworthy that apoptosis can be controlled by down regulating caspase3 activation [Ye et al, ] and increasing Bcl‐2 expression [Abdel Shakor et al, ]. MET treatment restored area% of bcl2 positive cells in cerebrum and sciatic nerve which was decreased in cerebellum and spinal cord of ACR + MET group.…”

Section: Discussionmentioning

confidence: 99%

Metformin Protects against Experimental Acrylamide Neuropathy in Rats

Oda

2017

Drug Development Research

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Preclinical Research To investigate the potential neuroprotective effects of metformin against experimental acrylamide neuropathy in rats, 24 rats were distributed into four equal groups (6 each). Group 1 was kept as a control. Group 2 (MET) was orally given metformin (200 mg/kg BW/day). Group 3 (ACR) was injected IP with acrylamide (50 mg/kg BW/day). Animals in group 4 (ACR + MET) were administered both MET and ACR at the same dose and route used in groups 2 and 3. Treatments were administered three times a week for three weeks. ACR induced an increase in lipid peroxidation in brain and spinal cord. This was associated with down regulation of bcl2 and up regulation of caspase3 in cerebrum, cerebellum, spinal cord, and sciatic nerve in the ACR-treated group. ACR-treated rats revealed neuronal degeneration and glial cell reaction in brain and spinal cord with axonal degeneration and myelin sheath irregularities in sciatic nerve. MET restored lipid peroxidation in brain and spinal cord, decreased caspase3 activity and up regulated bcl2 expression in cerebrum and sciatic nerve. Histopathological findings in ACR + MET group were lesser severe than those established in ACR-group indicating that MET ameliorates the neuropathic effects of ACR in rats. Drug Dev Res 78 : 349-359, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Metformin Protects against Experimental Acrylamide Neuropathy in Rats

Oda

2017

Drug Development Research

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“…To investigate how shikonin reduced liver injury by modulating the phosphorylation of JNK, we detected the expression of Bcl-2, Bax, and caspase 9. Bcl-2 and Bax belong to the Bcl-2 family, which is an antiapoptotic protein, while Bax represents a proapoptotic protein, and the balance of Bcl-2 and Bax determines cell survival or cell apoptosis [ 35 ] ( Figure 6 ). The phosphorylation of JNK results in the inactivation and phosphorylation of Bcl-2, leading to the release of cytochrome C and the activation of caspase-mediated apoptosis [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway

Liu

Xia

et al. 2016

Mediators of Inflammation

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Objective. Shikonin possesses anti-inflammatory effects. However, its function in concanavalin A-induced acute liver injury remains uncertain. The aim of the present study was to investigate the functions of shikonin and its mechanism of protection on ConA-induced acute liver injury. Materials and Methods. Balb/C mice were exposed to ConA (20 mg/kg) via tail vein injection to establish acute liver injury; shikonin (7.5 mg/kg and 12.5 mg/kg) was intraperitoneally administered 2 h before the ConA injection. The serum liver enzyme levels and the inflammatory cytokine levels were determined at 3, 6, and 24 h after ConA injection. Results. After the injection of ConA, inflammatory cytokines IL-1β, TNF-α, and IFN-γ were significantly increased. Shikonin significantly ameliorated liver injury and histopathological changes and suppressed the release of inflammatory cytokines. The expressions of Bcl-2 and Bax were markedly affected by shikonin pretreatment. LC3, Beclin-1, and p-JNK expression levels were decreased in the shikonin-pretreated groups compared with the ConA-treated groups. Shikonin attenuated ConA-induced liver injury by reducing apoptosis and autophagy through the inhibition of the JNK pathway. Conclusion. Our results indicated that shikonin pretreatment attenuates ConA-induced acute liver injury by inhibiting apoptosis and autophagy through the suppression of the JNK pathway.

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“…The Bcl-2 family can be divided into two types: one of which consists of anti-apoptotic proteins, including Bcl-2, Bcl-xL, Boo, CED-9, Bcl-w, Mcl-1, A1; the other consists of pro-apoptotic proteins, including Bax, Bak, Bad, Bcl-xs, Bid, Bok and Egl-1 [15,16,17]. The Bcl-2/Bax ratio is a decisive factor in cellular fate to a certain extent [18]. In the present study, pretreatment with PSS up-regulated the expression level of anti-apoptotic Bcl-2 and reduced the expression of Bax, indicating that PSS ameliorates inflammation by increasing the ability of cells to resist apoptosis and autophagy.…”

Section: Discussionmentioning

confidence: 99%

Propylene Glycol Alginate Sodium Sulfate Alleviates Cerulein‐Induced Acute Pancreatitis by Modulating the MEK/ERK Pathway in Mice

Zhang

et al. 2017

Marine Drugs

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Previous studies have focused on the effects of propylene glycol alginate sodium sulfate (PSS) against thrombosis, but the anti-inflammatory potential is unknown. Therefore, we specifically focused on the protective effects of PSS on cerulein-induced acute pancreatitis (AP) using a mouse model, and investigated the mechanism of PSS on autophagy and apoptosis via the Mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway. Cerulein (100 ug/kg) was used to induce AP by ten intraperitoneal injections at hourly intervals in Balb/C mice. Pretreatment with vehicle or PSS was carried out 1 h before the first cerulein injection and two doses (25 mg/kg and 50 mg/kg) of PSS were injected intraperitoneally. The severity of AP was assessed by pathological score, biochemistry, pro-inflammatory cytokine levels, myeloperoxidase (MPO) activity and MEK/ERK activity. Furthermore, pancreatic histological scores, serum amylase and lipase activities, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β interleukin (IL)-6 levels, and MPO activity were significantly reduced by PSS via up-regulated MEK/ERK activity. The representative molecules of apoptosis and autophagy, such as Bcl-2, Bax, Lc-3, Beclin-1, P62, were remarkably reduced. Taken together, these results indicate that PSS attenuates pancreas injury by inhibiting autophagy and apoptosis through a mechanism involving the MEK/ERK signaling pathway.

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Ceramide generation during curcumin-induced apoptosis is controlled by crosstalk among Bcl-2, Bcl-xL, caspases and glutathione

Cited by 20 publications

References 64 publications

Metformin Protects against Experimental Acrylamide Neuropathy in Rats

Metformin Protects against Experimental Acrylamide Neuropathy in Rats

Shikonin Attenuates Concanavalin A-Induced Acute Liver Injury in Mice via Inhibition of the JNK Pathway

Propylene Glycol Alginate Sodium Sulfate Alleviates Cerulein‐Induced Acute Pancreatitis by Modulating the MEK/ERK Pathway in Mice

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