Objective:To investigate the effect of equol on the proliferation of colom cancer cells and to explore the mechanisms.Methods: Colon cancer cells (DLD1,HCT15,COLO205,LOVO,SW480) were incubated, the cell proliferation was identified by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell proliferation assay.Reverse transcription PCR and Western blot were used to measure the mRNA and the protein expression of estrogen receptor and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)in the colon cancer cells, respectively.Moreover, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell proliferation assay was used to investigate the effect of estrogen receptor(ER) inhibitor,ERα agonist, and estrogen receptor ERβagonist on the cell proliferation.Results: ERα was faintly expressed in the DLD-1 and HCT-15 cells.However, ERβ expression in DLD1, HCT15, COLO205, LOVO, and SW480 colon cancer cells.Different concentrations of equol (0, 0.5, 1, 5, 10 μmol/L) significantly inhibited the growth of HCT-15 cell with the expression of ERα and ERβ.More-over, different concentrations of equol (0, 0.5, 1, 5, 10 μmol/L) significantly inhibited the growth of LOVO, and SW480 cells with the ERβ expression in a dose-dependent manner as demonstrated with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell proliferation assay.mRNA expressions of ERα and ERβ in HCT-15 were stimulated significantly.Western blotting proved that the protein expressions of ERα and ERβ increased with the increasing of equol dose.Moreover we found significant difference of Nrf2 protein expression in HCT-15 cell stimulated by different concentrationss of equol.After the similation of estrogen receptor inhibitor, ERα agonist, or ERβ agonist, we found that only dif-ferent concentrations of ERβ agonist(0, 1, 10, 100, 1 000, 10 000 nmol/L) significantly inhibited the growth of HCT-15, LOVO, and SW480 in adose-dependent manner.Estrogen receptor inhibitor and ERα agonistdid not present significant effect on the cell proliferation of HCT-15, LOVO, and SW480.Conclusion: Equol inhibited the colon cancer cell proliferation by its estrogenic activities and antioxidant activities.

Objective:To explore the treatment of pressure sores in different parts of the buttocks.Methods:From May, 2005 to March, 2020, 170 (157 patients) pressure sores in different parts of buttocks were treated. Eighty-two pressure sores located at sacrococcyx, 52 at ischial tuberosity, 24 at greater trochanter (without hip joint exposure) and 12 at femoral greater trochanter with exposure of the hip joint. Flaps were used to repair the pressure sores. ①Seventy-one sacrococcygeal pressure sores were repaired by the gluteal epithelial neurovascular flap; ②10 (10 patients) sacrococcygeal and 42 (36 patients) sciatic tubercle pressure sores were repaired by the posterior femoral neurovascular flap; ③24(24 patients) femoral trochanter pressure sores and 1(1 patient) sacrococcygeal pressure sore were repaired by the tensor fascia lata myocutaneous flap; ④2 (2 patients) sciatic tubercle pressure sores were repaired by the gracilis myocutaneous flap; ⑤12 (10 patients) femoral trochanter pressure sores were with hip joint exposure treated with hip joint amputation; ⑥8 (8 patients) pressure sores at ischial tuberosity were treated with VSD. The pressure sores were measured at 5.0 cm×8.0 cm-15.0 cm×30.0 cm, and the flaps were sized 10.0 cm×12.0 cm-17.0 cm×32.0 cm. The follow-up was conducted in 2 methods: visit of outpatient clinic by patients and WeChat distanced interview by medical staff.Results:The gluteal epithelial neurovascular flaps, tensor fasciae lata flaps, gracilis myocutaneous flaps and posterior femoral neurovascular flaps all survived; 4 of 10 posterior femoral neurovascular flaps had partial necrosis and healed after dressing change. A total of 139 patients were treated by flap repair, of which 136 pressure sores healed, except 1 sacrococcygeal pressure sore and 1 femoral greater trochanter pressure sore did not heal because the patient was in old age, long-term hypoproteinaemia and anaemia, and 1 ischial tubercle pressure sore failed to heal due to osteomyelitis osteomyelitis. Ten pressure sores at femoral greater trochanter decubitus with hip joint exposure treated by hip joint amputation and 8 pressure sores at ischial tubercle decubitus treated by simple insertion of VSD were all healed. The follow-up period was 0.5-15.0 years, 7.5 years in average. The results of follow-up showed that pressure sores healed without recurrence in 154 patients, but failed to heal in 3 patients.Conclusion:The gluteal epithelial neurotrophic vascular flap has reliable blood supply and is simple to harvest, and it is a good flap to repair sacrococcygeal pressure sores. The tensor fascia lata myocutaneous flap has reliable blood supply and is simple to harvest, hence it is a good flap to repair greater trochanteric pressure sores. Transposition of the posterior femoral cutaneous nerve nutrient vessel flap or the V-Y advancement flap is simple and effective in repair of the sciatic tuberosity pressure sores. However, it is not recommended to apply the transposition of posterior femoral cutaneous nerve nutrient vessel flap in repair of the sacrococcygobtaineal pressure sore, because it would cause a necrosis at the distal part of the flap. When a greater trochanteric pressure sore coexists with an expose of hip joint, the hip joint can be dissected. For the pressure sore at ischial tuberosity, and if there is a small wound with a large internal cavity, it can be treated with simple insertion of VSD.