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Hepatoprotective effect of total flavonoids of Mallotus apelta (Lour.) Muell.Arg. leaf against carbon tetrachloride-induced liver fibrosis in rats via modulation of TGF-β1/Smad and NF-κB signaling pathways.
J Ethnopharmacol. 2020 May 23; 254:112714.JE

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

The Mallotus apelta (Lour.) Muell.Arg. is a well-known traditional Chinese medicine (TCM) used for anti-inflammatory, hemostasis and chronic hepatitis.

AIM

The purpose of this study was to explore the antifibrotic effect of total flavonoids of Mallotus apelta leaf (TFM) and its potential mechanism.

METHODS

Hepatic fibrosis was induced by carbon tetrachloride (CCl4) in rats. The CCl4-induced rats received intragastric administration of colchicine (0.2 mg/kg per day), TFM (25, 50, 100 mg/kg per day) and the equal vehicle was given to normal rats. Pathological evaluation in hepatic tissue were examined by hematoxylin and eosin (HE) staining. And the levels of serum biochemical parameters were detected by automatic biochemical analysis. Meanwhile, the collagen deposition in liver was observed by staining with Masson's trichrome. Collagenic parameters and inflammatory factors were measured by enzyme-linked immunosorbent assay (ELISA) kits. Additionally, corresponding assay kit was used to estimate the antioxidant enzyme and lipid peroxidation. In order to explore the potential mechanism of anti-fibrotic effects in TFM, the expressions of liver fibrosis related gene and protein were analyzed by real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blot.

RESULTS

The CCl4-induced hepatic fibrosis were inhibited dose-dependently in rats by TFM. The results showed that the key hallmarks of liver injury including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), albumin (ALB) and total protein (TP) in the serum were reversed in CCl4-induced hepatic fibrosis rats which were treated by TFM. Furthermore, TFM significantly alleviates collagen accumulation and reduces the contents of hydroxyproline (Hyp), Type III precollagen (PC-III), collagen I (Col I), hyaluronic acid (HA) and laminin (LN). RT-PCR and Western blot results showed that TFM markedly inhibits liver fibrosis hallmark factor α-smooth muscle actin (α-SMA) expressions in CCl4-induced hepatic fibrosis rats. Moreover, TFM alleviated the oxidative stress and lipid peroxidation in rats induced by CCl4. TFM also attenuated the pro-inflammatory cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) via inhibiting nuclear factor-κB (NF-κB) activation. Meanwhile, transforming growth factor-β1 (TGF-β1)/Smad signaling pathway was inhibited by TFM treatment.

CONCLUSIONS

TFM can alleviate CCl4-induced hepatic fibrosis in rats, which potential mechanism may be due to its ability of reducing ECM accumulation, improving antioxidant and regulating TGF-β1/Smad signaling pathways and NF-κB-dependent inflammatory response.

Authors+Show Affiliations

Guangxi Medical University, Guangxi, China. Electronic address: zhang530021@163.com.Guangxi Medical University, Guangxi, China. Electronic address: 82564317@qq.com.Guangxi Medical University, Guangxi, China. Electronic address: 1147877815@qq.com.Guangxi Medical University, Guangxi, China. Electronic address: 670518680@qq.com.Guangxi Medical University, Guangxi, China. Electronic address: BFshing@163.com.Guangxi Medical University, Guangxi, China. Electronic address: 347800540@qq.com.Guangxi University of Chinese Medicine, Guangxi, China. Electronic address: hqj8@163.com.Guangxi Medical University, Guangxi, China. Electronic address: yong-ye@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32105750

Citation

Zhang, Bo, et al. "Hepatoprotective Effect of Total Flavonoids of Mallotus Apelta (Lour.) Muell.Arg. Leaf Against Carbon Tetrachloride-induced Liver Fibrosis in Rats Via Modulation of TGF-β1/Smad and NF-κB Signaling Pathways." Journal of Ethnopharmacology, vol. 254, 2020, p. 112714.
Zhang B, Lai L, Tan Y, et al. Hepatoprotective effect of total flavonoids of Mallotus apelta (Lour.) Muell.Arg. leaf against carbon tetrachloride-induced liver fibrosis in rats via modulation of TGF-β1/Smad and NF-κB signaling pathways. J Ethnopharmacol. 2020;254:112714.
Zhang, B., Lai, L., Tan, Y., Liang, Q., Bai, F., Mai, W., Huang, Q., & Ye, Y. (2020). Hepatoprotective effect of total flavonoids of Mallotus apelta (Lour.) Muell.Arg. leaf against carbon tetrachloride-induced liver fibrosis in rats via modulation of TGF-β1/Smad and NF-κB signaling pathways. Journal of Ethnopharmacology, 254, 112714. https://doi.org/10.1016/j.jep.2020.112714
Zhang B, et al. Hepatoprotective Effect of Total Flavonoids of Mallotus Apelta (Lour.) Muell.Arg. Leaf Against Carbon Tetrachloride-induced Liver Fibrosis in Rats Via Modulation of TGF-β1/Smad and NF-κB Signaling Pathways. J Ethnopharmacol. 2020 May 23;254:112714. PubMed PMID: 32105750.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hepatoprotective effect of total flavonoids of Mallotus apelta (Lour.) Muell.Arg. leaf against carbon tetrachloride-induced liver fibrosis in rats via modulation of TGF-β1/Smad and NF-κB signaling pathways. AU - Zhang,Bo, AU - Lai,Ling, AU - Tan,Yanjun, AU - Liang,Qiuyun, AU - Bai,Facheng, AU - Mai,Wanting, AU - Huang,Qiujie, AU - Ye,Yong, Y1 - 2020/02/24/ PY - 2019/04/21/received PY - 2019/10/06/revised PY - 2020/02/23/accepted PY - 2020/2/28/pubmed PY - 2021/1/6/medline PY - 2020/2/28/entrez KW - Anti-inflammatory KW - Hepatic fibrosis KW - Mallotus apelta KW - NF-κB KW - TGF-β1/smad SP - 112714 EP - 112714 JF - Journal of ethnopharmacology JO - J Ethnopharmacol VL - 254 N2 - ETHNOPHARMACOLOGICAL RELEVANCE: The Mallotus apelta (Lour.) Muell.Arg. is a well-known traditional Chinese medicine (TCM) used for anti-inflammatory, hemostasis and chronic hepatitis. AIM: The purpose of this study was to explore the antifibrotic effect of total flavonoids of Mallotus apelta leaf (TFM) and its potential mechanism. METHODS: Hepatic fibrosis was induced by carbon tetrachloride (CCl4) in rats. The CCl4-induced rats received intragastric administration of colchicine (0.2 mg/kg per day), TFM (25, 50, 100 mg/kg per day) and the equal vehicle was given to normal rats. Pathological evaluation in hepatic tissue were examined by hematoxylin and eosin (HE) staining. And the levels of serum biochemical parameters were detected by automatic biochemical analysis. Meanwhile, the collagen deposition in liver was observed by staining with Masson's trichrome. Collagenic parameters and inflammatory factors were measured by enzyme-linked immunosorbent assay (ELISA) kits. Additionally, corresponding assay kit was used to estimate the antioxidant enzyme and lipid peroxidation. In order to explore the potential mechanism of anti-fibrotic effects in TFM, the expressions of liver fibrosis related gene and protein were analyzed by real-time quantitative reverse transcription polymerase chain reaction (RT-PCR) and Western blot. RESULTS: The CCl4-induced hepatic fibrosis were inhibited dose-dependently in rats by TFM. The results showed that the key hallmarks of liver injury including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), albumin (ALB) and total protein (TP) in the serum were reversed in CCl4-induced hepatic fibrosis rats which were treated by TFM. Furthermore, TFM significantly alleviates collagen accumulation and reduces the contents of hydroxyproline (Hyp), Type III precollagen (PC-III), collagen I (Col I), hyaluronic acid (HA) and laminin (LN). RT-PCR and Western blot results showed that TFM markedly inhibits liver fibrosis hallmark factor α-smooth muscle actin (α-SMA) expressions in CCl4-induced hepatic fibrosis rats. Moreover, TFM alleviated the oxidative stress and lipid peroxidation in rats induced by CCl4. TFM also attenuated the pro-inflammatory cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) via inhibiting nuclear factor-κB (NF-κB) activation. Meanwhile, transforming growth factor-β1 (TGF-β1)/Smad signaling pathway was inhibited by TFM treatment. CONCLUSIONS: TFM can alleviate CCl4-induced hepatic fibrosis in rats, which potential mechanism may be due to its ability of reducing ECM accumulation, improving antioxidant and regulating TGF-β1/Smad signaling pathways and NF-κB-dependent inflammatory response. SN - 1872-7573 UR - https://www.unboundmedicine.com/medline/citation/32105750/Hepatoprotective_effect_of_total_flavonoids_of_Mallotus_apelta__Lour___Muell_Arg__leaf_against_carbon_tetrachloride_induced_liver_fibrosis_in_rats_via_modulation_of_TGF_β1/Smad_and_NF_κB_signaling_pathways_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-8741(19)31591-0 DB - PRIME DP - Unbound Medicine ER -