ObjectiveTo investigate the effect of solute carrier family 7 member 5 (SLC7A5) inhibitor JPH203 on renal fibrosis induced by unilateral ureteral obstruction in mice. MethodsSixteen SPF male C57BL/6 mice were randomly divided into the control group and the experimental group, with 8 mice in each group. The mouse model of renal fibrosis was established by unilateral ureteral obstruction. From the third day after surgery, the mice in the control group were intraperitoneally injected with phosphate-buffered saline (PBS) for 11 consecutive days, and the injection dose was 200 μL/d. Mice in the experimental group received intraperitoneal injection of JPH203 (50 mg/kg) every day for 11 days. On day 14, the mice were euthanized, then the kidney tissues were obtained. Hematoxylin and eosin (HE) staining was used to assess renal tissue damage, Masson staining was used to evaluate collagen fiber deposition in the extracellular matrix, and immunohistochemistry was used to detect the levels of fibroblast activation markers α-smooth muscle actin (α-SMA) and collagen type Ⅰ (COL-Ⅰ) in kidney tissues. Western blotting was further performed to measure the expression levels of SLC7A5 and transforming growth factor-β1 (TGF-β1), as well as the phosphorylation levels of mammalian target of rapamycin complex 1 (mTORC1) signaling pathway-related molecules. Real-time quantitative PCR was used to verify changes in the mRNA levels of SLC7A5, α-SMA, and COL-Ⅰ in kidney tissues. ResultsCompared with the control group, the experimental group showed reduced destruction of renal tissue structure and a significantly lower pathological injury score (P<0.05). Additionally, collagen deposition in the extracellular matrix was decreased, and the percentage of collagen fiber area was significantly reduced (P<0.001) in the experimental group. The levels of fibroblast activation markers α-SMA and COL-Ⅰ were significantly lower in the experimental group (both P<0.001). The expression levels of SLC7A5 and TGF-β1 were also significantly decreased (P<0.001), and the phosphorylation levels of mTORC1 signaling pathway-related proteins 4E-BP1 and mTORC1 were significantly reduced (P<0.001). Real-time quantitative PCR confirmed that the mRNA levels of SLC7A5, α- SMA, and COL-Ⅰ in kidney tissues were significantly lower in the experimental group (P<0.001). ConclusionJPH203 may inhibit the progression of renal fibrosis in mice by suppressing SLC7A5 expression, regulating the mTORC1 signaling pathway, and altering fibroblast activation status.

Objective To investigate the expression of signal transducer and activator of transcription 5 b (Stat5 b) and its phosphorylation (p-Stat5 b) in cervical lesions, its relationship with different degrees of cervical lesions, and its role in the pathogenesis and development of cervical lesions. Methods We obtained 80 specimens, including normal cervical tissues, low-grade squamous intraepithelial lesions (LSIL), high-grade squamous intraepithelial lesions (HSIL), and cervical cancer tissues. To analyze the correlation between Stat5 b and the degree of cervical lesions, immunohistochemical staining was performed to detect Stat5 b and p-Stat5 b expression. Results Increased Stat5 b expression had a positive correlation with the development of cervical lesions. The percentages of Stat5 b expressed in normal tissues, LSIL, HSIL, and cervical cancer tissues were 15.0％, 0.0％, 50.0％, and 80.0％, respectively, with significant differences among the groups (P ＜ 0.05). Conversely, the expression of p-Stat5 b had a negative correlation with the development of cervical lesions.Expression of p-Stat5 b in normal tissues, LSIL, HSIL, and cervical cancer tissues was 80.0％, 45.0％, 5.0％, and 0.0％, respectively, with statistically significant differences among the groups (P ＜ 0.05). Conclusion The expression of Stat5 b is significantly different in different degrees of cervical lesions, suggesting that Stat5 b signaling molecules may be involved in the development of cervical lesions.

Objective To investigate the effects of camel milk on immune cells in lamina propria (LP) of intestinal mucosa in mice. Methods Six male C57BL/6 mice(6-8 weeks) were randomly divided into two groups as follows: camel milk treatment group and double distilled water (DDW) control group. Samples of cells in LP of intestinal mucosa were collected. Cell counts and percentages of immune cells in LP were analyzed by flow cytometry. Levels of IL-4,IL-10,IL-17 and IFN-γ in the supernatants of cell cul-ture were measured by ELISA. Results Compared with the DDW control group, the camel milk treatment group showed increased percentage and absolute number of CD4+T cells as well as IFN-γ-secreting CD4+T cells in LP of intestinal mucosa(P<0.05). Moreover,significantly enhanced expression of IFN-γ and sup-pressed secretion of IL-4 were found in the camel milk treatment group (P<0.05). Conclusion Camel milk can promote the proliferation of CD4+T cells and enhance the secretion of IFN-γ,indicating that camel milk regulates the proliferation and cytokine secretion of immune cells in LP of intestinal mucosa in healthy mice.