Apocynin prevented inflammation and oxidative stress in carbon tetra chloride induced hepatic dysfunction in rats

Rahman, Mizanur; Muse, Awale Yousuf; Khan, D.M. Isha Olive; Ahmed, Ismaile Hussein; Subhan, Nusrat; Reza, Hasan Mahmud; Alam, Muhammad Ashraful; Nahar, Lutfun; Sarker, Satyajit D.

doi:10.1016/j.biopha.2017.05.101

Cited by 39 publications

(19 citation statements)

References 32 publications

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“…Oxidative stress reportedly induces different hepatic diseases including liver cirrhosis, cancer, ischemia, reperfusion injury as well as drug/chemical mediated hepatic toxicity [24]. In the present study, TD peel extract combated oxidative stress, diminished inflammation and fibrosis in the liver tissues, and restored the function of the antioxidant enzymes against CCl 4 -provoked liver damage in rats.…”

Section: Discussionsupporting

confidence: 54%

“…A further deterioration in the hepatic antioxidant defense systems has been shown by the substantial decline in CAT and SOD activities in the CCl 4 -administered rats, the two major enzymes supporting the antioxidant protection system of body causing progression from steatosis to steatohepatitis [24]. It has been reported that reduction of CAT and SOD levels and increase in CYP2E1 activity occur together which stimulate the generation of various free radicals and reactive intermediates, thus making the liver more vulnerable to oxidative stress-induced damages [47].…”

Section: Discussionmentioning

confidence: 99%

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Trichosanthes dioica Roxb. prevents hepatic inflammation and fibrosis in CCl4-induced ovariectomized rats

Khan

Rahman

Kabir

et al. 2020

Clinical Nutrition Experimental

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Plant-derived natural products have shown beneficial effects in many diseases associated with liver. The present study aimed to appraise the effects of Trichosanthes dioica (TD) peel extract on oxidative stress, inflammation as well as fibrosis exhibited by the ovariectomized rats in which hepatic damage had been induced by the administration of carbon tetrachloride (CCl 4). The CCl 4 administration in the ovariectomized rats elevated the plasma ALT, AST, and ALP level in comparison with the control while TD peel extract showed significant reduction of those activities. Besides, oxidative stress and lipid peroxidation also increased in CCl 4treated rats. TD peel extract significantly reduced the oxidative stress marker's concentration and improved the catalase and SOD activities in CCl 4-administered ovariectomized rats. These results suggest that TD peel extract is capable of protecting the liver from CCl 4 induced damage through preventing oxidative stress, lipid

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Trichosanthes dioica Roxb. prevents hepatic inflammation and fibrosis in CCl4-induced ovariectomized rats

Khan

Rahman

Kabir

et al. 2020

Clinical Nutrition Experimental

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“…4B and C). MDA is a lipid peroxidation product and is usually considered a reflection of cell injury (25). The present results showed that overexpressed miR-130a-3p or miR-301a-3p could ameliorate HG-induced MPC5 podocytes metabolic disturbance.…”

Section: Overexpressed Mir-130a-3p/301a-3p Inhibited Hg-induced Mpc5 supporting

confidence: 52%

Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling

Jiang

Wang²,

Liu

et al. 2017

Exp Ther Med

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Abstract. Tumor necrosis factor (TNF)-α has been reported to be important in glomerulonephritis, which is closely associated with podocyte dysfunction and apoptosis. However, the precise mechanisms by which TNF-α expression are regulated remain unclear. The purpose of the present study was to investigate the role of microRNA (miR)-130a-3p/301a-3p in the post-transcriptional control of TNF-α expression and high glucose (HG)-induced podocyte dysfunction. Mice MPC5 podocytes were incubated with HG and transfected with miR-130a-3p/301a-3p mimics or inhibitors, reactive oxygen species (ROS) levels were measured by flow cytometry assay, and the mRNA and protein levels were assayed by using reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The targeted genes were predicted by a bioinformatics algorithm and verified using a dual luciferase reporter assay. It was observed that miR-130a-3p/301a-3p was a novel regulator of TNF-α in mouse podocytes. miR-130a-3p/301a-3p mimics inhibited TNF-α 3'-untranslated region luciferase reporter activity, in addition to endogenous TNF-α protein expression. Furthermore, forced expression of miR-130a-3p or miR-301a-3p resulted in the downregulation of ROS and malondialdehyde (MDA) and the upregulation of superoxide dismutase (SOD) 1 in the presence of HG. Inhibition of TNF-α level prevented a remarkable reduc tion in SOD activity and a marked increase in ROS and MDA levels in HG-treated podocytes. Furthermore, TNF-α loss-of-function significantly reversed HG-induced podocyte apoptosis. These data demonstrated a novel up-stream role for miR-130a-3p/301a-3p in TNF-α-mediated podocyte dysfunction and apoptosis in the presence of HG. IntroductionGlomerular podocytes are highly differentiated cells that play a key role in maintaining the integrity of the glomerular filtration barrier (1). In glomerular diseases, podocyte damage leads to increased glomerular barrier pore size, allowing the passage of proteins or other mediators to the tubular lumen, which results in proteinuria and progressive loss of kidney function (2). Accumulating evidence indicates that hyperglycemia contributes to podocyte lesions (3). Clinical data demonstrate that podocyte integrity is impaired, and the decreased podocyte number is confirmed in individuals with type 1 (T1DM) and 2 diabetes mellitus (T2DM) (4,5). In cultured podocytes, high glucose induces apoptosis, epithelial-mesenchymal transition (EMT), mitochondrial fission and autophagy through different signaling pathways (6-9). However, the underlying molecular mechanisms of high glucose-induced MPC5 podocytes dysfunction remain to be fully elucidated.MicroRNAs (miRs) are endogenous, noncoding, short, single-stranded RNAs (18-25 nucleotides) that are evolutionarily highly conserved, believed to regulate the translation of target messenger RNAs (mRNAs) by binding to its 3'-untranslated regions (3'-UTRs) and verified to play a role in controlling a variety of biological processes (10). Recently, several studies have h...

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“…Although, early antiviral therapy can reverse liver fibrosis in patients with HBV and HCV infection (D'Ambrosio et al, ; Marcellin et al, ), for other causes of liver fibrosis and cirrhosis, there are still no effective anti‐fibrosis drugs applied to clinical treatment (Sun & Kisseleva, ), Therefore, developing anti‐liver fibrosis drugs is highly significant (Lee, Wallace, & Friedman, ). We used fibrotic rats as research subjects, and apocynin (AP) (Rahman et al, ) as a positive control, and we observe the effect of UA intervention (UA prevention and treatment) on reversing liver fibrosis. Compared to the liver fibrosis group, the fibrous septum and collagen deposition were reduced in the liver tissue of the UA prevention and treatment group (Figure a–d).…”

Section: Discussionmentioning

confidence: 99%

Ursolic acid ameliorates CCl4‐induced liver fibrosis through the NOXs/ROS pathway

Gan

Zhang

Huang

et al. 2018

Journal Cellular Physiology

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Liver fibrosis is a reversible wound‐healing response that occurs after liver injury. NADPH oxidases (NOXs) and reactive oxygen species (ROS) which are expressed in hepatocytes (HCs), hepatic stellate cells (HSCs), and Kupffer cells (KCs) play an important role in the development of hepatic fibrosis. In in vitro studies, we had shown that ursolic acid (UA) could reverse liver fibrosis by inhibiting the activation of NOX‐mediated fibrotic signaling networks in HSCs. In this study, we verified that UA could alleviate CCl4‐induced liver fibrosis by reducing the expression of NOXs/ROS in HCs, HSCs, KCs. Meanwhile, the phagocytic index α and clearance index K which represent phagocytosis of KCs were unchanged. Together, all our data demonstrated that UA induced the proliferation of HCs, promoted apoptosis in HSCs, and prevented activation of KCs in vivo by reducing the expression of NOXs/ROS in HCs, HSCs, KCs. Besides, UA had no effect on the host defense function.

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Apocynin prevented inflammation and oxidative stress in carbon tetra chloride induced hepatic dysfunction in rats

Cited by 39 publications

References 32 publications

Trichosanthes dioica Roxb. prevents hepatic inflammation and fibrosis in CCl4-induced ovariectomized rats

Trichosanthes dioica Roxb. prevents hepatic inflammation and fibrosis in CCl4-induced ovariectomized rats

Overexpression of miR‑130a‑3p/301a‑3p attenuates high glucose‑induced MPC5 podocyte dysfunction through suppression of TNF‑α signaling

Ursolic acid ameliorates CCl4‐induced liver fibrosis through the NOXs/ROS pathway

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