Objective To study the effect and mechanism of Weishen decoction on bone protection in senescence-accelerated mouse prone 6 (SAMP6). Methods Thirty SAMP6 mice were randomly divided into SOP model group, calcium carbonate + calcitol group and Weishen decoction group. Ten SAMR1 mice aged normally were used as normal control group. Weishen decoction group was given Weishen thick decoction , calcium carbonate + calcitol group was given calcium carbonate D3 and alpha calcitol suspension, SOP model group and normal control group were given the same volume of normal saline. After 3 months of treatment, serum and femur were taken. Bone mineral density, bone histopathology, bone metabolism, TGF-β, Smad2 pathway protein, MAPK pathway p-JNK, p-ERK, p38, NF-κB p65, p50 proteins were detected. Result Compared with the normal control group, the bone trabeculae of the mice with bone disorder in SOP model group were reduced. There were significant differences in bone mineral density, calcium (Ca), phosphorus (P), bone alkaline phosphatase (BALP), tartrate-resistant acid phosphatase (TRACP), procollagen type I N-terminal propeptide (P1NP), signaling pathway TGF-β, Smad2, p-JNK, p-ERK, p38, p65 and p50 proteins compared with normal control group (P<0.01). Compared with SOP model group, the bone structure of Weishen decoction group was improved, bone mineral density and bone metabolism indexes Ca, BALP and P1NP were significantly increased (P<0.01), and the protein expressions of TGF-β, Smad2, p-JNK, p-ERK and p38 were significantly increased (P<0.01). P and TRACP were decreased (P<0.01), p65 and p50 proteins were decreased (P<0.01). Compared with calcium carbonate + calcitol group, P1NP was significantly increased (P<0.01), TRACP was decreased (P<0.01), TGF-β, Smad2, P-JNK, P-ERK and p38 proteins were significantly increased (P<0.01), and p65 and p50 proteins were decreased (P < 0.01) in Weishen decoction group. Conclusion Weishen decoction can improve bone cell activity, regulate bone metabolism, promote bone formation and increase bone density by regulating TGF-β/Smad2 and MAPK pathways. |