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Page 1 od 163 rezultati
[Effect of berberine hydrochloride on the expression of interleukin-1beta and tumor necrosis factor-alpha in periodontal tissues in rats].
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OBJECTIVE
To determine the effects of berberine hydrochloride on the expressions of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in periodontal tissues in rat periodontitis model.
METHODS
Based on the successful rat periodontitis model, the experimental rats were
Berberine suppresses inflammatory agents-induced interleukin-1beta and tumor necrosis factor-alpha productions via the inhibition of IkappaB degradation in human lung cells.
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Pulmonary inflammation is a characteristic of many lung diseases. Increased levels of pro-inflammatory cytokines, such as interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), have been correlated with lung inflammation. In this study, we demonstrated that various inflammatory
Berberine inhibits tumor necrosis factor-α-induced expression of inflammatory molecules and activation of nuclear factor-κB via the activation of AMPK in vascular endothelial cells.
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Berberine, which is a well‑known drug used in traditional medicine, has been demonstrated to exert diverse pharmacological effects, including anti‑inflammatory effects. However, whether berberine can affect the production of inflammatory molecules in vascular endothelial cells remains to be
Acetaldehyde-induced interleukin-1beta and tumor necrosis factor-alpha production is inhibited by berberine through nuclear factor-kappaB signaling pathway in HepG2 cells.
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Alcoholic liver disease (ALD) is one of the most common liver diseases in the world. Increased levels of proinflammatory cytokines, including interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), have been correlated with the patients affected by ALD. However, the direct effect
Berberine-antiproliferative activity in vitro and induction of apoptosis/necrosis of the U937 and B16 cells.
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Berberine, an isoquinoline plant alkaloid, is widely distributed in plants used in the traditional Chinese medicine. It displays a wide range of biological activities and the mechanism of action. Our previous studies of the anticancer activity of berberine against the cancer cell lines HeLa and
Inhibition of p38 mitogen-activated protein kinase potentiates the apoptotic effect of berberine/tumor necrosis factor-related apoptosis-inducing ligand combination therapy.
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It was previously reported that berberine (BBR) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) exhibited a synergistic apoptotic effect on triple negative breast cancer (TNBC) cells. In addition, the BBR/TRAIL combination treatment sensitized TRAIL-resistant TNBC cells to
Mitochondrial protein cyclophilin-D-mediated programmed necrosis attributes to berberine-induced cytotoxicity in cultured prostate cancer cells.
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The prostate cancer is one of the leading causes of men's cancer mortality. The development of alternative chemotherapeutic strategies is urgent. Berberine has displayed significant anti-prostate cancer activities. The underlying mechanisms are not fully understood. In the current study, we found
Berberine enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in breast cancer.
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Berberine (BBR) has been used for the treatment of bacterial and fungal infections and also for cancer-associated symptoms such as diarrhea. Furthermore, it has been reported that BBR may have direct antitumor effects. Although evidence supports the theory that tumor necrosis factor (TNF)-related
Effect of berberine on proinflammatory cytokine production by ARPE-19 cells following stimulation with tumor necrosis factor-α.
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OBJECTIVE
Berberine (BBR) is a well-known drug used in traditional medicine and has been shown to possess anti-inflammatory properties. Whether it can affect the production of inflammatory cytokines by RPE cells is not yet clear and was therefore the subject of our study.
METHODS
ARPE-19 cells were
Berberine attenuates cAMP-induced lipolysis via reducing the inhibition of phosphodiesterase in 3T3-L1 adipocytes.
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Berberine, a hypoglycemic agent, has been shown to decrease plasma free fatty acids (FFAs) level in insulin-resistant rats. In the present study, we explored the mechanism responsible for the antilipolytic effect of berberine in 3T3-L1 adipocytes. It was shown that berberine attenuated lipolysis
Resolution of liver fibrosis by isoquinoline alkaloid berberine in CCl₄-intoxicated mice is mediated by suppression of oxidative stress and upregulation of MMP-2 expression.
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Liver fibrosis is the result of chronic liver injury, and it represents a widespread medical problem. The aim of this study is to investigate the antifibrotic activity of isoquinoline alkaloid berberine in carbon tetrachloride (CCl₄)-induced damage in mice. Hepatic fibrosis was induced by
[Effect of Berberine on the Insulin Resistance and TLR4/IKKbeta/NF-kappaB Signaling Pathways in Skeletal Muscle of Obese Rats with Insulin Resistance].
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OBJECTIVE
To explore the possible mechanism of berberine improve insulin resistance in skeletal muscle of obese rats.
METHODS
Forty Wistar rats were divided into normal control group (NC group, n =10) and high fat food group (HF group, n=30). After the obese model rats established successfully, the
Berberine ameliorates lipopolysaccharide‑induced inflammatory responses in mouse inner medullary collecting duct‑3 cells by downregulation of NF‑κB pathway.
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The major role of inner medullary collecting duct (IMCD) cells is to maintain water and sodium homeostasis. In addition to the major role, it also participates in the protection of renal and systemic inflammation. Although IMCD cells could take part in renal and systemic inflammation, investigations
Berberine regulates peroxisome proliferator-activated receptors and positive transcription elongation factor b expression in diabetic adipocytes.
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Berberine has hypoglycemic and hypolipidemic effects on diabetic rats. This study investigated the relationship between hypoglycemic and hypolipidemic effects of berberine and peroxisome proliferator-activated receptors (PPARs) and positive transcription elongation factor b (P-TEFb) (including
Berberine (BBR) Attenuated Palmitic Acid (PA)-Induced Lipotoxicity in Human HK-2 Cells by Promoting Peroxisome Proliferator-Activated Receptor α (PPAR-α).
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BACKGROUND Berberine (BBR), a natural alkaloid isolated from Coptis chinensis, has frequently been reported as an antidiabetic reagent, partly due to its lipid-lowering activity. Evidence suggests that BBR ameliorates palmitate-induced lipid deposition and apoptosis in renal tubular epithelial cells
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