Gremlin is a bone morphogenic protein (BMP) antagonist and is elevated in diabetic kidney tissues. In the early course of diabetic nephropathy (DN), podocyte are injured. We studied the protein and gene expression of gremlin in mice podocytes cultured in hyperglycemia ambient. The role of gremlin on podocyte injury and the likely signaling pathways involved were determined. Expression of gremlin was visualized by confocal microscopy. Recombinant mouse gremlin and small interfering RNA (siRNA) targeting to gremlin1 identified the role played by gremlin on podocytes. Study of canonical (smad2/3) and non-canonical (p38MAPK and JNK1/2) transforming growth factor beta (TGFβ)/smad mediated signaling revealed the putative signaling mechanisms involved. Smad2/3 siRNA and TGFβ receptor inhibition (SB431542) were used to probe canonical TGFβ/smad signaling in gremlin-induced podocyte injury. Apoptosis of podocytes was measured by TUNEL assay. Gremlin expression was enhanced in high glucose cultured mouse podocytes, and was localized predominantly in the cytoplasm and negligibly on the cell membrane. Not only expression of nephrin and synaptopodin were decreased on treatment with gremlin, but also synaptopodin rearrangement and nephrin relocalization were evident. Knockdown gremlin1 or smad2/3 by siRNA, and inhibition of TGFβR (SB431542) attenuated podocyte injury. Inhibition of canonical TGF-β signal blocked the injury of gremlin on podocytes. In conclusion, gremlin was clearly elevated in high glucose cultured mouse podocytes, and likely employed endogenous canonical TGFβ1/Smad signaling to induce podocyte injury. Knockdown gremlin1 by siRNA may be clinically useful in the attenuation of podocyte injury.

Intrauterine adhesions (IUA) may be caused by endometrial stromal cell proliferation, increases in myofibroblasts or increases in extracellular matrix secretion. However, the specific mechanisms underlying the development of IUA have yet to be elucidated. The present study identified that angiotensin (Ang) II is capable of promoting endometrial epithelium cell (EEC) proliferation and the transdifferentiation of EECs into myofibroblasts. Furthermore, the present study found that Ang II increased the expression of the myofibroblast specific protein α-smooth muscle actin (α-SMA), decreased the expression and secretion of E-cadherin, and increased the synthesis of collagen type I (Col I) and fibronectin (FN). However, Ang-(1–7) was observed to inhibit Ang II-induced proliferation and transdifferentiation of EECs, decrease the expression of α-SMA, increase the expression of E-cadherin and decrease the synthesis and secretion of Col I and FN. These findings suggest that Ang-(1–7) is capable of inhibiting the Ang II-induced proliferation and transdifferentiation of human EECs and decreases in Col I and FN secretion. The present study may provide insight into the mechanism underlying endometrial fibrosis.

Lycium barbarum polysaccharide (LBP) is the main active component of Lycium barbarum and has many beneficial effects, including neuroprotection, antiaging, and antioxidation. This study mainly explores the immunomodulatory effect of Lycium barbarum polysaccharides against liver fibrosis based on the intelligent medical Internet of Things. This measure emphasizes that the current effective methods and methods for the treatment of liver cancer are mainly combined treatments of Western medicine and Chinese medicine. These treatments have a certain effect in preventing liver cancer, reducing recurrence, and reducing side effects. Among them, chemotherapy has unique advantages in improving the quality of life and prolonging survival. With the development of medical science and technology, the clinical efficacy and efficacy of traditional Chinese medicine in the treatment of liver cancer are constantly improving. The mechanism is also studied from many aspects. The treatment time of LBPs on fibrotic hepatocytes was set to 24 h. Take liver fiber cells in logarithmic growth phase and incubate them at 37°C for 24 h. The whole process uses a temperature sensor for intelligent temperature control. In the experiment, groups of LBPs with different concentrations and different molecular weight ranges were set up and each group had 6 multiple holes. The original medium was aspirated and replaced with a medium containing different concentrations of LBPs (12.5, 25, 50, 100, and 200 μg/mL) and cultured for 24 h. Based on the previous research, this study used in vitro cell experiments, microscopic observation, and MTT method to verify whether Lycium barbarum polysaccharides inhibit the proliferation of human liver cancer cells in vitro and whether they cooperate with the chemotherapy drug fluorouracil to play a tumor-killing effect. Animal experiments, using ELISA, HE staining, and other methods, explore the molecular and immunological mechanisms of LBP’s antiliver cancer effect from the perspective of Th/Th2 differentiation balance and DC function, in order to provide experimental evidence for Chinese medicine polysaccharides in cancer immunotherapy and application. At different LBP concentrations (0 μmol/L, 5 μmol/L, 10 μmol/L, and 15 μmol/L), the inhibition rates were 0.80%, 20.06%, 35.44%, and 55.39%, respectively. This study provides a new method for large-scale expansion of hepatocytes in vitro, laying a stronger foundation for biological treatment of liver fibrosis.

Previous studies have shown that Lycium barbarum polysaccharides (LBPs) serve an important role in antioxidant activity to protect the cells and tissues. However, the specific mechanism of LBPs in the prevention of endometrial damage remains to be elucidated. Using morphological observation, cell proliferation assay, the detection of superoxide dismutase (SOD) activity and the content of malondialdehyde (MDA) in cell culture supernatant fluid, the detection by western blot analysis and reverse transcription-quantitative polymerase chain reaction of the mRNA and protein expression levels of caspase‑3 and Bcl‑2 in endometrial stromal cells (ESCs), it was demonstrated that, in vitro, hydrogen peroxide (H2O2)-induced death of ESCs, increased the content of MDA and decreased the activity of SOD, and decreased the expression of Bcl-2 and increased the expression of caspase‑3. LBPs can inhibit H2O2‑induced cell death of ESCs, decrease the content of MDA in ESCs and increase the activity of SOD, as well as increasing the expression of Bcl‑2 and decreasing the expression levels of caspase‑3. These findings suggested that LBPs can inhibit H2O2‑induced apoptosis of EECs and that LBPs are able to offer a significant protection against oxidative stress to ESCs.

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