Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Tytuł pozycji:

Melittin Inducing the Apoptosis of Renal Tubule Epithelial Cells through Upregulation of Bax/Bcl-2 Expression and Activation of TNF- α Signaling Pathway.

Tytuł:
Melittin Inducing the Apoptosis of Renal Tubule Epithelial Cells through Upregulation of Bax/Bcl-2 Expression and Activation of TNF- α Signaling Pathway.
Autorzy:
Shu Y; Kidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.; Division of Nephrology, The Third People's Hospital of Chengdu, Chengdu, Sichuan 610031, China.
Yang Y; Kidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Zhao Y; Kidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Ma L; Kidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Fu P; Kidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Wei T; Kidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Zhang L; Kidney Research Institute, Division of Nephrology, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
Źródło:
BioMed research international [Biomed Res Int] 2019 May 29; Vol. 2019, pp. 9450368. Date of Electronic Publication: 2019 May 29 (Print Publication: 2019).
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: New York, NY : Hindawi Pub. Co.
MeSH Terms:
Apoptosis/*drug effects
Epithelial Cells/*drug effects
Kidney Tubules, Proximal/*drug effects
Melitten/*pharmacology
Proto-Oncogene Proteins c-bcl-2/*metabolism
Signal Transduction/*drug effects
Tumor Necrosis Factor-alpha/*metabolism
bcl-2-Associated X Protein/*metabolism
Acute Kidney Injury/pathology ; Animals ; Cell Line ; Disease Models, Animal ; Epithelial Cells/pathology ; Humans ; In Situ Nick-End Labeling ; Kidney Tubules, Proximal/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Up-Regulation
References:
Crit Care Med. 2012 Jul;40(7):2116-23. (PMID: 22710204)
J Coll Physicians Surg Pak. 2014 Nov;24 Suppl 3:S209-10. (PMID: 25518776)
Clin Tech Small Anim Pract. 2006 Nov;21(4):194-204. (PMID: 17265905)
J Urol. 2008 Dec;180(6):2694-700. (PMID: 18951565)
J Surg Res. 2017 Jun 15;214:69-78. (PMID: 28624062)
Exp Cell Res. 2017 Oct 1;359(1):138-144. (PMID: 28778797)
Int J Biochem Cell Biol. 2000 Nov-Dec;32(11-12):1123-36. (PMID: 11137452)
Int Immunopharmacol. 2017 Jun;47:134-140. (PMID: 28391160)
Curr Opin Nephrol Hypertens. 2002 May;11(3):301-8. (PMID: 11981260)
Nature. 2000 Oct 12;407(6805):770-6. (PMID: 11048727)
Arch Toxicol. 2004 Mar;78(3):147-55. (PMID: 14551673)
Nephrol Dial Transplant. 2010 Apr;25(4):1146-50. (PMID: 19934093)
Apoptosis. 2016 Jun;21(6):721-36. (PMID: 26979714)
Int Urol Nephrol. 2018 Jun;50(6):1171-1180. (PMID: 29368247)
Clin J Am Soc Nephrol. 2013 Nov;8(11):1850-6. (PMID: 24009218)
Adv Exp Med Biol. 2016;930:1-23. (PMID: 27558815)
Case Rep Nephrol. 2017;2017:8596981. (PMID: 28706746)
Clin J Am Soc Nephrol. 2013 Sep;8(9):1482-93. (PMID: 23744003)
South Med J. 2011 May;104(5):378-9. (PMID: 21606727)
Toxicol Appl Pharmacol. 2016 Dec 15;313:104-108. (PMID: 27984128)
Kidney Int. 2013 Mar;83(3):372-6. (PMID: 23302721)
Apoptosis. 2008 Jan;13(1):11-32. (PMID: 17968659)
Am J Physiol Renal Physiol. 2017 Oct 1;313(4):F926-F937. (PMID: 28424210)
J Assoc Physicians India. 2014 Aug;62(8):738-40. (PMID: 25856951)
Nat Rev Mol Cell Biol. 2010 Sep;11(9):621-32. (PMID: 20683470)
J Med Case Rep. 2014 Jun 13;8:188. (PMID: 24929921)
Chin Med J (Engl). 2012 Jun;125(11):2070-2. (PMID: 22884081)
Med J Malaysia. 2012 Feb;67(1):133-5. (PMID: 22582570)
Substance Nomenclature:
0 (Proto-Oncogene Proteins c-bcl-2)
0 (Tumor Necrosis Factor-alpha)
0 (bcl-2-Associated X Protein)
114100-40-2 (Bcl2 protein, mouse)
20449-79-0 (Melitten)
Entry Date(s):
Date Created: 20191128 Date Completed: 20200413 Latest Revision: 20220411
Update Code:
20240104
PubMed Central ID:
PMC6854966
DOI:
10.1155/2019/9450368
PMID:
31772938
Czasopismo naukowe
Background: Acute kidney injury (AKI) caused by bee stings is common, with characteristics of acute onset, severe illness, and high mortality. Melittin, a major component of bee venom, has been considered to play a key role in bee sting related AKI. This study aims to illustrate whether melittin could lead to apoptosis of renal tubular epithelial cells (RTECs) and to investigate its mechanism.
Methods: In vivo, 45 mice were randomly divided into the melittin group (n=30, injected with melittin into the tail vein according to the total dose of 4.0 ug/g weight) and the control group (n=15, injected with the same volume of saline into the tail vein). In vitro, human RTECs (HK-2) were cultured and treated with melittin (2ug/ml or 4ug/ml) and TNF- α (10ng/ml). Biochemical analysis, HE stains, and electron microscope were performed to evaluate renal function and pathological changes. TUNEL stains and flow cytometry were performed to detect apoptosis. Real-time PCR was performed to detect mRNA levels of Bax, Bcl-2, and TNF- α . Simple western assay and immunohistochemical (IH) and immunofluorescent (IF) stains were performed for protein detection.
Results: Melittin successfully induced AKI in mice. Compared with the control group, obvious injury and apoptosis of RTECs were observed in the melittin group; the mRNA and protein expressions of Bax were significantly increased, while the expression of Bcl-2 was significantly decreased. The serum TNF- α level in melittin group was significantly higher than that in control group. In vitro, the results confirmed that melittin can cause HK-2 cells apoptosis. The trends of expression of Bax and Bcl-2 were consistent with the results in vivo. The levels of TNF- α mRNA and protein by PCR and Western blot were significantly higher in melittin group than those in control group.
Conclusion: Melittin can lead to the apoptosis of RTECs, which may be mediated by upregulating the expression of Bax/Bcl-2 and activating the TNF- α signaling pathway.
Competing Interests: The authors declare no conflicts of interest.
(Copyright © 2019 Ying Shu et al.)
Zaloguj się, aby uzyskać dostęp do pełnego tekstu.

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies