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Anti-fibrotic effect of natural toxin bee venom on animal model of unilateral ureteral obstruction.

An HJ, Kim KH, Lee WR, Kim JY, Lee SJ, Pak SC, Han SM, Park KK - Toxins (Basel) (2015)

Bottom Line: However, BV treatment markedly reduced these reactions compared with untreated UUO mice.The expression levels of TNF-α and IL-1β were significantly reduced in BV treated mice compared with UUO mice.In conclusion, BV may be a useful therapeutic agent for the prevention of fibrosis that characterizes progression of chronic kidney disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, College of Medicine, Catholic University of Daegu, 3056-6, Daemyung-4-Dong, Nam-gu, Daegu 705-718, Korea. ahj119@cu.ac.kr.

ABSTRACT
Progressive renal fibrosis is the final common pathway for all kidney diseases leading to chronic renal failure. Bee venom (BV) has been widely used as a traditional medicine for various diseases. However, the precise mechanism of BV in ameliorating the renal fibrosis is not fully understood. To investigate the therapeutic effects of BV against unilateral ureteral obstruction (UUO)-induced renal fibrosis, BV was given intraperitoneally after ureteral ligation. At seven days after UUO surgery, the kidney tissues were collected for protein analysis and histologic examination. Histological observation revealed that UUO induced a considerable increase in the number of infiltrated inflammatory cells. However, BV treatment markedly reduced these reactions compared with untreated UUO mice. The expression levels of TNF-α and IL-1β were significantly reduced in BV treated mice compared with UUO mice. In addition, treatment with BV significantly inhibited TGF-β1 and fibronectin expression in UUO mice. Moreover, the expression of α-SMA was markedly withdrawn after treatment with BV. These findings suggest that BV attenuates renal fibrosis and reduces inflammatory responses by suppression of multiple growth factor-mediated pro-fibrotic genes. In conclusion, BV may be a useful therapeutic agent for the prevention of fibrosis that characterizes progression of chronic kidney disease.

No MeSH data available.


Related in: MedlinePlus

BV attenuates the expression of TGF-β1 and fibronectin in obstructed kidneys. (A) Immunohistochemical staining for TGF-β1 and fibronectin in the kidneys at seven days after UUO surgery. (B,C) Immunohistochemical staining was used to evaluate the extent of fibrotic genes, which was subsequently quantified. (D) Western blot analysis shows that BV suppresses the protein expression of TGF-β1 and fibronectin in UUO kidneys. (E) RT-PCR results show that BV suppresses the mRNA expression of TGF-β1 and fibronectin in UUO kidneys. GAPDH levels were analyzed as an internal control. Representative images from each study group. Magnification 400×. Results are expressed as means ± SE of three independent determinations. *p < 0.05 vs. NC group. †p < 0.05 vs. UUO group.
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toxins-07-01917-f003: BV attenuates the expression of TGF-β1 and fibronectin in obstructed kidneys. (A) Immunohistochemical staining for TGF-β1 and fibronectin in the kidneys at seven days after UUO surgery. (B,C) Immunohistochemical staining was used to evaluate the extent of fibrotic genes, which was subsequently quantified. (D) Western blot analysis shows that BV suppresses the protein expression of TGF-β1 and fibronectin in UUO kidneys. (E) RT-PCR results show that BV suppresses the mRNA expression of TGF-β1 and fibronectin in UUO kidneys. GAPDH levels were analyzed as an internal control. Representative images from each study group. Magnification 400×. Results are expressed as means ± SE of three independent determinations. *p < 0.05 vs. NC group. †p < 0.05 vs. UUO group.

Mentions: UUO initially produces inflammation, which gradually progresses to fibrosis in the kidney with increased expression of cytokines, such as TGF-β1 [12]. During the development of fibrosis, TGF-β1 expression is upregulated and is known to promote fibrosis under a variety of circumstances, including ECM remodeling [13]. The ECM protein fibronectin is focally deposited in renal fibrosis, where it contributes to inflammatory signaling [14]. As shown in Figure 3A, TGF-β1 and fibronectin positive cells are limited to the tubular basement membranes of the non-obstructed kidney, whereas large amounts of those cells are present in the interstitial space of the obstructed kidney. The cells positive for TGF-β1 and fibronectin were increased in UUO mice, but they were decreased by BV treatment. These observations were confirmed through Western blotting and RT-PCR. The expression of TGF-β1 and fibronectin was increased in UUO, however this increase was abolished by BV treatment (Figure 3D,E). These results suggest that BV effectively blocks fibrotic changes and suppresses the accumulation of ECM in obstructive kidneys.


Anti-fibrotic effect of natural toxin bee venom on animal model of unilateral ureteral obstruction.

An HJ, Kim KH, Lee WR, Kim JY, Lee SJ, Pak SC, Han SM, Park KK - Toxins (Basel) (2015)

BV attenuates the expression of TGF-β1 and fibronectin in obstructed kidneys. (A) Immunohistochemical staining for TGF-β1 and fibronectin in the kidneys at seven days after UUO surgery. (B,C) Immunohistochemical staining was used to evaluate the extent of fibrotic genes, which was subsequently quantified. (D) Western blot analysis shows that BV suppresses the protein expression of TGF-β1 and fibronectin in UUO kidneys. (E) RT-PCR results show that BV suppresses the mRNA expression of TGF-β1 and fibronectin in UUO kidneys. GAPDH levels were analyzed as an internal control. Representative images from each study group. Magnification 400×. Results are expressed as means ± SE of three independent determinations. *p < 0.05 vs. NC group. †p < 0.05 vs. UUO group.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4488681&req=5

toxins-07-01917-f003: BV attenuates the expression of TGF-β1 and fibronectin in obstructed kidneys. (A) Immunohistochemical staining for TGF-β1 and fibronectin in the kidneys at seven days after UUO surgery. (B,C) Immunohistochemical staining was used to evaluate the extent of fibrotic genes, which was subsequently quantified. (D) Western blot analysis shows that BV suppresses the protein expression of TGF-β1 and fibronectin in UUO kidneys. (E) RT-PCR results show that BV suppresses the mRNA expression of TGF-β1 and fibronectin in UUO kidneys. GAPDH levels were analyzed as an internal control. Representative images from each study group. Magnification 400×. Results are expressed as means ± SE of three independent determinations. *p < 0.05 vs. NC group. †p < 0.05 vs. UUO group.
Mentions: UUO initially produces inflammation, which gradually progresses to fibrosis in the kidney with increased expression of cytokines, such as TGF-β1 [12]. During the development of fibrosis, TGF-β1 expression is upregulated and is known to promote fibrosis under a variety of circumstances, including ECM remodeling [13]. The ECM protein fibronectin is focally deposited in renal fibrosis, where it contributes to inflammatory signaling [14]. As shown in Figure 3A, TGF-β1 and fibronectin positive cells are limited to the tubular basement membranes of the non-obstructed kidney, whereas large amounts of those cells are present in the interstitial space of the obstructed kidney. The cells positive for TGF-β1 and fibronectin were increased in UUO mice, but they were decreased by BV treatment. These observations were confirmed through Western blotting and RT-PCR. The expression of TGF-β1 and fibronectin was increased in UUO, however this increase was abolished by BV treatment (Figure 3D,E). These results suggest that BV effectively blocks fibrotic changes and suppresses the accumulation of ECM in obstructive kidneys.

Bottom Line: However, BV treatment markedly reduced these reactions compared with untreated UUO mice.The expression levels of TNF-α and IL-1β were significantly reduced in BV treated mice compared with UUO mice.In conclusion, BV may be a useful therapeutic agent for the prevention of fibrosis that characterizes progression of chronic kidney disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, College of Medicine, Catholic University of Daegu, 3056-6, Daemyung-4-Dong, Nam-gu, Daegu 705-718, Korea. ahj119@cu.ac.kr.

ABSTRACT
Progressive renal fibrosis is the final common pathway for all kidney diseases leading to chronic renal failure. Bee venom (BV) has been widely used as a traditional medicine for various diseases. However, the precise mechanism of BV in ameliorating the renal fibrosis is not fully understood. To investigate the therapeutic effects of BV against unilateral ureteral obstruction (UUO)-induced renal fibrosis, BV was given intraperitoneally after ureteral ligation. At seven days after UUO surgery, the kidney tissues were collected for protein analysis and histologic examination. Histological observation revealed that UUO induced a considerable increase in the number of infiltrated inflammatory cells. However, BV treatment markedly reduced these reactions compared with untreated UUO mice. The expression levels of TNF-α and IL-1β were significantly reduced in BV treated mice compared with UUO mice. In addition, treatment with BV significantly inhibited TGF-β1 and fibronectin expression in UUO mice. Moreover, the expression of α-SMA was markedly withdrawn after treatment with BV. These findings suggest that BV attenuates renal fibrosis and reduces inflammatory responses by suppression of multiple growth factor-mediated pro-fibrotic genes. In conclusion, BV may be a useful therapeutic agent for the prevention of fibrosis that characterizes progression of chronic kidney disease.

No MeSH data available.


Related in: MedlinePlus