Mechanism of allicin for improvement of hepatic fibrosis by regulating autophagy
By: Xiaoyan, Chen
.
Contributor(s): Bin, Cao.
Publisher: Bangalore Association of Pharmaceutical Teachers of India (APTI) 2022Edition: Vol.56(4), Oct-Dec.Description: 1099-1105p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
Indian journal of pharmaceutical education and researchSummary: Objectives: To explore the effects of allicin on the expression of mitochondrial autophagy-
related proteins in liver tissues of hepatic fibrosis (HF) rats. Materials and Methods:
45 SD rats were randomly divided into Normal, Model, Low, Middle and High groups.
The HF rat model was replicated intraperitoneal injection of carbon tetrachloride and
ethanol gavage for 4 weeks. Detection of alanine aminotransferase (ALT) and aspartate
aminotransferase (AST) in rat serum; HE and Masson staining to observe pathological
changes; Evaluating LC 3B protein expression by Immunofluorescence; Western Blotting
and qRT-PCR methods were used to detect PINK1, Parkin, Beclin 1, and LC3 gene and
protein expression levels in rat liver tissues. Results: Compared with the Normal group,
the degree of HF in the model group was obvious, the volume fraction of collagen
increased significantly (
p<0.001), the LC 3B protein expression significantly up-
regulation (
p<0.001), and the rat serum ALT and AST increased significantly (
p<0.001,
respectively). Up-regulation of PINK1, Parkin, Beclin 1, and LC 3B mRNA and protein
expression and LC 3II/LC 3I ratio in liver tissues (
p<0.001, respectively); Compared with
the model group, Allicin treated groups had reduced HF degree, collagen volume fraction
decreased significantly (
p<0.05, respectively), LC 3B protein was significantly reduced
(
p<0.05, respectively), and liver tissue PINK1, Parkin, Beclin 1, and LC3B mRNA and
protein expressions, and LC 3II/LC 3I ratio were down-regulated (
p<0.05, respectively).
Conclusion: Allicin could improve hepatic fibrosis. The mechanism might be related to
down-regulating the expression of PINK1, Parkin, Beclin 1, and LC 3 gene and proteins
and interfering with the level of mitochondrial autophagy.
| Item type | Current location | Call number | Status | Date due | Barcode | Item holds |
|---|---|---|---|---|---|---|
Articles Abstract Database
|
School of Pharmacy Archieval Section | Not for loan | 2023-0107 |
Objectives: To explore the effects of allicin on the expression of mitochondrial autophagy-
related proteins in liver tissues of hepatic fibrosis (HF) rats. Materials and Methods:
45 SD rats were randomly divided into Normal, Model, Low, Middle and High groups.
The HF rat model was replicated intraperitoneal injection of carbon tetrachloride and
ethanol gavage for 4 weeks. Detection of alanine aminotransferase (ALT) and aspartate
aminotransferase (AST) in rat serum; HE and Masson staining to observe pathological
changes; Evaluating LC 3B protein expression by Immunofluorescence; Western Blotting
and qRT-PCR methods were used to detect PINK1, Parkin, Beclin 1, and LC3 gene and
protein expression levels in rat liver tissues. Results: Compared with the Normal group,
the degree of HF in the model group was obvious, the volume fraction of collagen
increased significantly (
p<0.001), the LC 3B protein expression significantly up-
regulation (
p<0.001), and the rat serum ALT and AST increased significantly (
p<0.001,
respectively). Up-regulation of PINK1, Parkin, Beclin 1, and LC 3B mRNA and protein
expression and LC 3II/LC 3I ratio in liver tissues (
p<0.001, respectively); Compared with
the model group, Allicin treated groups had reduced HF degree, collagen volume fraction
decreased significantly (
p<0.05, respectively), LC 3B protein was significantly reduced
(
p<0.05, respectively), and liver tissue PINK1, Parkin, Beclin 1, and LC3B mRNA and
protein expressions, and LC 3II/LC 3I ratio were down-regulated (
p<0.05, respectively).
Conclusion: Allicin could improve hepatic fibrosis. The mechanism might be related to
down-regulating the expression of PINK1, Parkin, Beclin 1, and LC 3 gene and proteins
and interfering with the level of mitochondrial autophagy.
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