To observe the effects of "three manipulations and three acupoints" tuina on the recovery of motor function in rats with sciatic nerve injury, and to explore its mechanism.

Twenty-four male SD rats were randomly divided into four groups using a random number table method: normal, sham operation, model, and tuina groups, with six rats per group. The normal group received no intervention, whereas only the sciatic nerve was exposed in the sham operation group. In the model and tuina groups, the sciatic nerve was clamped and injured to create a rat model of sciatic nerve injury, simulating peripheral nerve injury in clinical settings. The normal group was not intervened. On the seventh day after modeling, the sham operation and model groups were given grip restraint; in the tuina group, a tuina manipulation simulator was used to apply an intervention involving "three manipulations and three acupoints," and the point-pressing, kneading, and plucking methods were applied on "Yinmen" (BL37), "Chengshan" (BL57), and "Yanglingquan" (GB34) in turn. The rats were rested for one day after 10 days of intervention, and the total intervention time was 20 days. Before modeling and after intervention, a grip strength test system was used to measure the grip strength of the hind limbs. After intervention, an automated gait analysis system was used to assess the gait of rats (walking duration, maximum contact area, and swing phase duration), and the sciatic function index (SFI) was calculated; a biological signal acquisition and analysis system was used to determine the sciatic nerve conduction velocity and surface electromyography (sEMG) signals (amplitude and incubation period) of the gastrocnemius muscle; the morphology, number, and area of motor endplate (MEP) at the neuromuscular junction (NMJ) of the gastrocnemius muscle were examined using the cupric ferrocyanide method; the concentrations of acetylcholine (ACh) and acetylcholinesterase (AChE) at the NMJ of the gastrocnemius muscle were detected using an enzyme-linked immunosorbent assay.

Compared with the normal and sham operation groups, the model group showed a decrease in hind limb grip strength (P<0.05); compared with the model groups, the tuina group exhibited an increase in hind limb grip strength (P<0.05). Compared with the normal and sham operation groups, the model group showed reductions in walking duration, maximum contact area, SFI, and gastrocnemius muscle sEMG amplitude (P<0.05); compared with the model group, the tuina group demonstrated increases in these indicators (P<0.05). Compared with the normal and sham operation groups, the model group showed increases in swing phase duration and gastrocnemius muscle sEMG incubation period (P<0.05); compared with the model group, the tuina group showed decreases in these indicators (P<0.05). Compared with the normal and sham operation groups, the model group showed lighter MEP staining, along with decreases in MEP number and area at the NMJ of the gastrocnemius muscle (P<0.05); compared with the model group, the tuina group exhibited darker MEP staining, as well as increases in MEP number and area (P<0.05). Compared with the normal and sham operation groups, the model group had lower concentrations of ACh and AChE at the NMJ of the gastrocnemius muscle (P<0.05); compared with the model group, the tuina group showed higher levels of these biomarkers (P<0.05).

Tuina can improve motor function in rats with sciatic nerve injury. Its mechanism may involve enhancing the efficiency of electrical signal conduction, increasing the sensitivity of chemical signal transmission at the NMJ, promoting nerve repair and regeneration, and modulating the reinnervation of muscles by nerves.

To investigate the effects of “Three Methods and Three Acupoints” (TMTP) Tuina therapy on spinal microcirculation in sciatic nerve injury (SNI).

Thirty-six Sprague–Dawley rats were randomly assigned to four groups: normal, sham operation, model, and TMTP Tuina. Successful model induction was confirmed by observable hind limb lameness. After 20 sessions, hind limb grip strength and motor nerve conduction velocity (MNCV) were measured at baseline and following the 10th and 20th intervention. CD31 and α-SMA in the ventral horn of SNI model rats were detected using immunofluorescence. Motor neurons in the ventral horn were detected by Nissl staining. PTEN levels in the ventral horn were measured by ELISA, and PI3K, Akt, BDNF, VEGF, and HIF-1α expression was determined by RT-PCR. Spinal cord microcirculation was evaluated by western blotting analysis of the levels of Akt, p-Akt, BDNF, and VEGF.

Hind limb grip strength and MNCV significantly improved in the TMTP Tuina group compared to the model group (both P <.001). Morphology of ventral horn motor neurons in the TMTP Tuina group improved compared to the model group, with increased expressions of α-SMA (P =.002) and CD31 (P =.006). Western blot analysis indicated increased expression of VEGF (P =.005), p-Akt (P <.001), and BDNF (P =.008) in the ventral horn following Tuina treatment. RT-PCR analysis revealed increased expression of PI3K, Akt, BDNF, VEGF and HIF-1α (all P <.05). In contrast, expression of PTEN decreased compared to the model group (P <.001).

TMTP Tuina therapy may restore motor function in rats, enhance ventral horn motor neuron morphology, and promote angiogenesis and vascular smooth muscle proliferation. The mechanism may involve the activation of the PI3K/Akt signaling pathway.

To investigate the changes in the hypothalamic metabolites of lipopolysaccharide (LPS) febrile young rabbits after the treatment with pediatric tuina.

A total of 30 young rabbits were randomly assigned into three groups: the normal group, the model group, and the tuina group. Both the model group and the tuina group were injected intravenously with LPS. “Six antipyretic manipulations” (pushing Tianmen, pushing Kangong, kneading Taiyang, kneading Erhougaogu, clearing Tianheshui, and pushing Jizhu) were administered 1 h after the LPS injection in the tuina group. The rectal temperatures of the young rabbits were monitored during the experiment to explore the antipyretic effect. Three hours after the injection, the content of interleukin-1β (IL-1β), tumor necrosis factor (TNF)-α, and prostaglandin E₂ (PGE₂) in the serum was detected. In addition, liquid chromatography-mass spectrometry (LC-MS) was used for the hypothalamus metabolomics.

Compared with the model group, the rectal temperature of the tuina group was decreased at 2 h and 3 h after the LPS injection (P = .04, P = .03, respectively), and the content of IL-1β, TNF-α, and PGE₂ was decreased (P = .03, P = .003, and P = .008, respectively). The metabolomics results showed that there were 23 potential biomarkers after the tuina intervention, enriching 27 pathways. Lipid metabolites, especially glycerophospholipids, were a majority of the altered metabolites. The primary metabolic pathways affected by tuina included the arachidonic acid metabolism, the GABAergic synapse, d-glutamine and d-glutamate metabolism, and the glutamatergic synapse.

Pediatric tuina reduced the temperature of the febrile rabbits and downregulated the expression of IL-1β, TNF-α, and PGE₂, and the antipyretic mechanism may be related to changes in metabolites and metabolic pathways in the hypothalamus.