The aim of this study was to investigate the possible protective role of hydrogen-rich saline solution (HRSS) and WR-2721 on the testicular damage induced by irradiation. Sprague-Dawley rats were randomly divided into four groups. Group I served as control group. Rats in group II were exposed to the irradiation. The animals in group III and IV were injected intraperitoneally with HRSS (5 ml/kg) and WR-2721 (200 mg/kg), respectively, 15 min. before the start of gamma irradiation. Testis weight, testis dimensions, sperm count, sperm motility, apoptosis index and biochemical assays were assessed after a 4-day initiation of irradiation. Testis weight, testis dimensions, sperm count, sperm motility in group II were significantly lower compared with those in the control group, whereas they were higher in the HRSS and WR-2721 group. Apoptosis index was significantly increased in group II. Treatment of rats with HRSS and WR-2721 significantly reduced the apoptosis index. On the other hand, irradiation markedly decreased activities of SOD. Activities of SOD were significantly improved when treated with HRSS and WR-2721. Significant increase in the MDA level was observed in group II. MDA levels of group III and IV were significantly lowered when compared with group II. HRSS also played a significant role in the recovery of serum testosterone levels. The results from this experimental study suggest that hydrogen has a possible protective effect against radiation-induced testicular damage.

Tendon stem cells (TSCs), recently identified as tendon cells, play an important role in maintaining the homeostasis of tendon tissue. Age-related decrease in the function of TSCs has been reported. Recent reports demonstrated that hypoxic condition is advantageous for efficient expansion of TSCs. Moreover, the impaired function of aged stem cells could be modulated by exposing them to a young environment. Therefore, we investigated the effects of hypoxic-conditioned culture medium (HCCM) from young TSCs on the proliferation, migration, senescence, and tenocyte phenotype of aged TSCs. TSCs were isolated, and the conditioned medium was collected. There were 4 groups: young TSCs, aged TSCs, aged TSCs + aged HCCM, and aged TSCs + young HCCM. The proliferative capacity, migration, β-galactosidase activity, and tenogenic differentiation potential of TSCs were assessed. Our results showed that HCCM enhanced the proliferation and migration potential of aged TSCs. Moreover, the senescence-associated β-galactosidase activity of aged TSCs was decreased by young HCCM. After being cultured in the young HCCM, the expressions of tenocyte-related genes in aged TSCs were significantly enhanced. Together, results of this study indicate that HCCM from young TSCs may represent an effective strategy to improve the impaired function of aged TSCs.

Our study demonstrates that NaHS protects against UUO-induced renal damage via attenuating fibrosis, oxidative stress, and inflammation. Therefore, H2 S may be useful as a potential candidate in the treatment of renal damage induced by obstruction. Neurourol. Urodynam. 33:538-543, 2014. © 2013 Wiley Periodicals, Inc.

The aim of this study was to examine the effectiveness of HGF in blocking TGF-beta1-induced collagen III and alpha-smooth muscle actin (alpha-SMA) production in rat healing fibroblasts, fibroblasts were obtained from healing medial collateral ligament (MCL) injury. Cell culture was supplemented with 5 ng/ml of TGF-beta1 along with increasing doses of HGF (10-40 ng/ml). The productions of collagen III in supernatants culture were assayed by enzyme-linked immunosorbent assay. Expression of alpha-SMA was assessed by Western blot. Treatment with TGF-beta1 significantly stimulated collagen III and alpha-SMA production in healing fibroblasts. Remarkably, the addition of HGF reduced productions of all components induced by TGF-beta1 in a dose-dependent manner. This study shows that HGF antagonizes the action of TGF-beta1 effectively in cultured healing MCL injury fibroblasts. The results provide a cellular and molecular basis for HGF's acting as a therapeutic agent for MCL scar formation and poor healing.

We examined the effectiveness of hepatocyte growth factor (HGF) in blocking production of transforming growth factor (TGF)-beta1-induced collagen I, fibronectin, and alpha-smooth muscle actin (alpha-SMA) in the flexor tendon sheath of rabbits in vitro. Fibroblasts were obtained from the sheaths. Cell culture was supplemented with TGF-beta1 5 ng/ml and increasing doses of HGF (10-40 ng/ml). The production of collagen I and fibronectin in supernatants culture were examined using an enzyme-linked immunosorbent assay (ELISA). alpha-SMA expression was assessed by western blot. TGF-beta1 stimulated production of collagen I, fibronectin, and alpha-SMA greatly, while HGF significantly (p<0.05) reduced production of all components induced by TGF-beta1 in a dose-dependent manner. This suggests that HGF effectively antagonises the action of TGF-beta1 in cultured fibroblasts from flexor tendon sheaths. The results provide a cellular and molecular basis for HGF acting as a therapeutic agent for adhesions in flexor tendons.