PMID- 36975512
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230330
IS  - 1467-3045 (Electronic)
IS  - 1467-3037 (Print)
IS  - 1467-3037 (Linking)
VI  - 45
IP  - 3
DP  - 2023 Mar 8
TI  - Serratiopeptidase Attenuates Lipopolysaccharide-Induced Vascular Inflammation by 
      Inhibiting the Expression of Monocyte Chemoattractant Protein-1.
PG  - 2201-2212
LID - 10.3390/cimb45030142 [doi]
AB  - Lipopolysaccharide (LPS) has potent pro-inflammatory properties and acts on many 
      cell types including vascular endothelial cells. The secretion of the cytokines 
      MCP-1 (CCL2), interleukins, and the elevation of oxidative stress by 
      LPS-activated vascular endothelial cells contribute substantially to the 
      pathogenesis of vascular inflammation. However, the mechanism involving 
      LPS-induced MCP-1, interleukins, and oxidative stress together is not well 
      demonstrated. Serratiopeptidase (SRP) has been widely used for its 
      anti-inflammatory effects. In this research study, our intention is to establish 
      a potential drug candidate for vascular inflammation in cardiovascular disorder 
      conditions. We used BALB/c mice because this is the most successful model of 
      vascular inflammation, suggested and validated by previous research findings. Our 
      present investigation examined the involvement of SRP in vascular inflammation 
      caused by lipopolysaccharides (LPSs) in a BALB/c mice model. We analyzed the 
      inflammation and changes in the aorta by H&E staining. SOD, MDA, and GPx levels 
      were determined as per the instructions of the kit protocols. ELISA was used to 
      measure the levels of interleukins, whereas immunohistochemistry was carried out 
      for the evaluation of MCP-1 expression. SRP treatment significantly suppressed 
      vascular inflammation in BALB/c mice. Mechanistic studies demonstrated that SRP 
      significantly inhibited the LPS-induced production of proinflammatory cytokines 
      such as IL-2, IL-1, IL-6, and TNF-alpha in aortic tissue. Furthermore, it also 
      inhibited LPS-induced oxidative stress in the aortas of mice, whereas the 
      expression and activity of monocyte chemoattractant protein-1 (MCP-1) decreased 
      after SRP treatment. In conclusion, SRP has the ability to reduce LPS-induced 
      vascular inflammation and damage by modulating MCP-1.
FAU - Yadav, Vikas
AU  - Yadav V
AUID- ORCID: 0000-0002-0278-4828
AD  - Department of Pharmacology and Toxicology, National Institute of Pharmaceutical 
      Education and Research, Hajipur 844102, Bihar, India.
FAU - Sharma, Satyam
AU  - Sharma S
AUID- ORCID: 0000-0001-6364-3810
AD  - Department of Pharmacology and Toxicology, National Institute of Pharmaceutical 
      Education and Research, Hajipur 844102, Bihar, India.
FAU - Kumar, Ashutosh
AU  - Kumar A
AD  - Department of Pharmacology and Toxicology, National Institute of Pharmaceutical 
      Education and Research, Kolkata 700054, West Bengal, India.
AD  - Department of Pharmacology and Toxicology, National Institute of Pharmaceutical 
      Education and Research, Sahibzada Ajit Singh Nagar 160062, Punjab, India.
FAU - Singh, Sanjiv
AU  - Singh S
AUID- ORCID: 0000-0002-9021-6547
AD  - Department of Pharmacology and Toxicology, National Institute of Pharmaceutical 
      Education and Research, Hajipur 844102, Bihar, India.
FAU - Ravichandiran, V
AU  - Ravichandiran V
AD  - Department of Pharmacology and Toxicology, National Institute of Pharmaceutical 
      Education and Research, Hajipur 844102, Bihar, India.
LA  - eng
PT  - Journal Article
DEP - 20230308
PL  - Switzerland
TA  - Curr Issues Mol Biol
JT  - Current issues in molecular biology
JID - 100931761
PMC - PMC10047379
OTO - NOTNLM
OT  - lipopolysaccharides
OT  - monocyte chemoattractant protein-1
OT  - oxidative stress
OT  - serratiopeptidase
OT  - vascular inflammation
OT  - vascular smooth muscle cells
COIS- The authors declare no conflict of interest.
EDAT- 2023/03/29 06:00
MHDA- 2023/03/29 06:01
PMCR- 2023/03/08
CRDT- 2023/03/28 09:14
PHST- 2022/11/11 00:00 [received]
PHST- 2022/11/29 00:00 [revised]
PHST- 2023/02/01 00:00 [accepted]
PHST- 2023/03/29 06:01 [medline]
PHST- 2023/03/28 09:14 [entrez]
PHST- 2023/03/29 06:00 [pubmed]
PHST- 2023/03/08 00:00 [pmc-release]
AID - cimb45030142 [pii]
AID - cimb-45-00142 [pii]
AID - 10.3390/cimb45030142 [doi]
PST - epublish
SO  - Curr Issues Mol Biol. 2023 Mar 8;45(3):2201-2212. doi: 10.3390/cimb45030142.