Muscle Grip Strength Research Articles

Influence of Physical Exercise on the Rehabilitation of Volumetric Muscle Loss Injury Reconstructed with Autologous Adipose Tissue.

In volumetric muscle loss (VML) injuries, spontaneous muscle regeneration capacity is limited. The implantation of autologous adipose tissue in the affected area is an option to treat these lesions; however, the effectiveness of this therapy alone is insufficient for a complete recovery of the damaged muscle. This study examined the influence of treadmill exercise on the rehabilitation of VML injuries reconstructed with autologous adipose tissue, as a strategy to counteract the limitations of spontaneous regeneration observed in these injuries. Forty adult male Wistar rats were divided into eight groups of five individuals each: normal control (NC), regenerative control (RC), VML control (VML), VML injury reconstructed with fresh autologous adipose tissue (FAT), exercise-rehabilitated control (RNC), exercise-rehabilitated regenerative control (RRC), exercise-rehabilitated VML injury (RVML), and exercise-rehabilitated VML injury reconstructed with fresh autologous adipose tissue (RFAT). Histological and histochemical staining techniques were used for the analysis of structural features and histomorphometric parameters of the tibialis anterior muscle. Grip strength tests were conducted to assess muscle force. Exercise rehabilitation decreased the proportion of disoriented fibers in RFAT vs. FAT group. The percentage of fibrosis was significantly higher in FAT and RFAT groups versus NC and RNC groups but did not vary significantly between FAT and RFAT groups. Overall, muscle grip strength and fiber size increased significantly in the exercise-rehabilitated groups compared to control groups. To conclude, rehabilitation with physical exercise tended to normalize the process of muscle repair in a model of VML injury reconstructed with fresh autologous adipose tissue, but it did not reduce the intense fibrosis associated with these injuries.

Supplementation with a phenolic-rich fraction from Ilex kudingcha improves inflammatory stress, gastrocnemius weights, and foreleg muscle grip strength in murine squamous cell carcinoma (SCC7)-bearing mice

Ethanol supernatant of Ilex kudingcha methanol extract (ESIKME) was identified to be rich in phenolic compounds and inhibited murine squamous cell carcinoma (SCC)-7 growth through slightly restoring adaptive immunity and Th1-inclination immune balance in the SCC7-bearing mice. To further evaluate the inhibitory effects and mechanisms of ESIKME against SCC7-induced inflammation status, the effects of ESIKME on inflammatory stress and related cachexia induced by SCC7 cells were investigated in vitro and in vivo. Chemical components of ESIKME were measured using an advanced LC-MS/MS analysis. SCC7 cells were treated with mouse splenocyte (SCM) and macrophage conditioned media (MCM) cultured without/with ESIKME in vitro. SCC7-bearing mice were orally administered with ESIKME for 26 days in vivo. Cachexia-related biomarkers in the SCC7-bearing mice were analyzed. Most of the detected compounds in ESIKME were polymeric or oxidized phenolic compounds. Either SCM or MCM without ESIKME significantly inhibited SCC7 cell growth. The high-dose ESIKME-administered group (400 mg/kg b.w./day) had significantly higher body weights, feed efficiency, and energy efficiency than the dietary control (DC) group, suggesting non-adverse toxic effects for ESIKME supplementation in the SCC7-bearing mice. The DC group had a higher TNF-α and TNF-α/IL-10 secretion ratio but lower anti-inflammatory IL-10 cytokine secretions by macrophages than the vehicle control group. ESIKME administration dose-dependently and significantly reversed these adverse statuses. Medium dose ESIKME (100 mg/kg b.w./day) decreased tumor sizes but increased gastrocnemius weights and foreleg muscle grip strength. Our results suggest that ESIKME alleviated inflammatory stress and related cachexia in vitro and in vivo.

Inhibition of CERS1 in skeletal muscle exacerbates age-related muscle dysfunction.

Age-related muscle wasting and dysfunction render the elderly population vulnerable and incapacitated, while underlying mechanisms are poorly understood. Here, we implicate the CERS1 enzyme of the de novo sphingolipid synthesis pathway in the pathogenesis of age-related skeletal muscle impairment. In humans, CERS1 abundance declines with aging in skeletal muscle cells and, correlates with biological pathways involved in muscle function and myogenesis. Furthermore, CERS1 is upregulated during myogenic differentiation. Pharmacological or genetic inhibition of CERS1 in aged mice blunts myogenesis and deteriorates aged skeletal muscle mass and function, which is associated with the occurrence of morphological features typical of inflammation and fibrosis. Ablation of the CERS1 orthologue lagr-1 in Caenorhabditis elegans similarly exacerbates the age-associated decline in muscle function and integrity. We discover genetic variants reducing CERS1 expression in human skeletal muscle and Mendelian randomization analysis in the UK biobank cohort shows that these variants reduce muscle grip strength and overall health. In summary, our findings link age-related impairments in muscle function to a reduction in CERS1, thereby underlining the importance of the sphingolipid biosynthesis pathway in age-related muscle homeostasis.

Inhibition of CERS1 in skeletal muscle exacerbates age-related muscle dysfunction

Age-related muscle wasting and dysfunction render the elderly population vulnerable and incapacitated, while underlying mechanisms are poorly understood. Here, we implicate the CERS1 enzyme of the de novo sphingolipid synthesis pathway in the pathogenesis of age-related skeletal muscle impairment. In humans, CERS1 abundance declines with aging in skeletal muscle cells and, correlates with biological pathways involved in muscle function and myogenesis. Furthermore, CERS1 is upregulated during myogenic differentiation. Pharmacological or genetic inhibition of CERS1 in aged mice blunts myogenesis and deteriorates aged skeletal muscle mass and function, which is associated with the occurrence of morphological features typical of inflammation and fibrosis. Ablation of the CERS1 orthologue lagr-1 in Caenorhabditis elegans similarly exacerbates the age-associated decline in muscle function and integrity. We discover genetic variants reducing CERS1 expression in human skeletal muscle and Mendelian randomization analysis in the UK biobank cohort shows that these variants reduce muscle grip strength and overall health. In summary, our findings link age-related impairments in muscle function to a reduction in CERS1, thereby underlining the importance of the sphingolipid biosynthesis pathway in age-related muscle homeostasis.

The memory ameliorating effects of novel N-benzyl pyridine-2-one derivatives on scopolamine-induced cognitive deficits in mice

BackgroundAlzheimer's disease (AD), the most common form of progressive dementia in the elderly, is a chronic neurological disorder that decreases cognitive ability. Although the underlying cause of AD is yet unknown, oxidative stress and brain acetylcholine shortage are the key pathogenic causes.ResultsThe current study shows that these derivatives have the potential to improve memory in mice by inhibiting scopolamine-induced acetylcholinesterase activity, oxidative and nitrosative stress, and improving locomotor activity and muscle grip strength in the rota rod test. When compared to the illness control, the memory-enhancing potential of novel N-benzyl pyridine-2-one derivatives was highly significant (P < 0.0001).ConclusionsThe observed memory ameliorating effect of novel N-benzyl pyridine-2-one makes them as a a good choice for treatment of individuals with cognitive impairment.Graphical abstract

Evaluating Motor Dysfunction and Oxidative Stress Induced by Trichloroethylene in Wistar Rats.

Trichloroethylene, a chlorinated solvent widely used as a degreasing agent, is a common environmental contaminant. Emerging evidence suggests that chronic exposure to trichloroethylene (TCE) contributes to the development of Parkinson's disease (PD). TCE induced LRRK2 kinase activity in the rat brain and produced a significant dopaminergic lesion in the nigrostriatal tract with elevated oxidative stress. Here we have utilized TCE-induced PD model for the assessment of test drug. Oral gavage administration of TCE at a dose of 1000mg/kg/day for 6weeks was utilized to induced PD. Muscle grip strength was estimated by rotarod and grid performance test. Motor activity by actophotometer and locomotor stability were assessed by forelimb locomotor scale (FLS) and forelimb step alternation test (FSAT). However, the postural stability was assessed by postural stability test (PST). Biochemical estimation consists of determination of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), GSH level (reduced glutathione), and nitrite concentration.

Study of the Combined Effect of Silymarin, Quercetin, and Hesperidin on 3 nitro Propionic Acid-induced Rat Model of Huntington’s Disease

This investigation proposes to encapsulate how the combined effects of silymarin, quercetin, and hesperidin impact the abilities of rats with Huntington’s disease (HD). Male Wistar rats were administered 3-NP through intraperitoneal injections. Various behavioral measures, including muscle grip strength, locomotor activity, and a string test, were assessed. After 22 days, assessments of lipid peroxidation, glutathione levels, superoxide dismutase, catalase, succinate dehydrogenase (Complex II) activity, lactate dehydrogenase (Complex IV) activity, and the determination of interleukin-6 levels was performed. Administering 3-NP dosage of 10 mg/kg body weight for 21 days outcomes in a substantial rise in learning and memory impairments that closely resembled those seen in HD. Within specific treatment groups, it was observed that quercetin significantly enhanced muscle coordination and demonstrated a noteworthy upsurge in various behavioral measures. After silymarin, quercetin, and hesperidin were combined, there were significant improvements in key biochemical markers such as glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and SDH activity induced by 3-NP. These improvements led to a decrease in neuronal damage and apoptosis in brain. Each bioflavonoid successfully reinstated the stages of biochemical markers, for example, GSH, SOD, CAT, and SDH, while reducing the activity of malondialdehyde (MDA) and lactate dehydrogenase (LDH). However, after these bioflavonoids were combined, their collective impact was more potent Compared to what each achieved individually.

Perch essence prevents cell death to improve skeletal muscle mass and strength: Evidence from in vitro and human model

Background:Fish protein supplementation may maintain muscle strength and prevent sarcopenia as it contains a complex array of macro- and micronutrients essential for building the skeletal muscle. Objective:The aim of this study was to evaluate the influence of perch essence (PE) supplementation on muscle mass and muscle function of through human and cell model. Methods:The open label clinical trial was conducted to assess the therapeutic effect of PE on muscle mass improvement. The mouse skeletal muscle cell (C2C12) model of muscle atrophy was analyzed for cell viability. Results:Our results showed PE contained abundant branched chain amino acid, taurine, hydroxyproline and collagen. After one month of supplementation with PE in our human model, there was a significant increase in muscle mass in the whole body and all parts of the body, with an increase of 1.55 % in the whole body, 1.79% in the trunk, 1.64% in the arms and 1.38% in the legs. The percentage of subcutaneous fat in the trunk, arms and legs also decreased significantly by 2.49%, 3.21% and 3.40% respectively. PE supplementation also improves muscle grip strength, especially with the dominant hand. The cell model results demonstrated that PE could effectively prevent skeletal muscle cell from death induced by dexamethasone. Conclusion:This study suggests that the branched chain amino acids, taurine, hydroxyproline and collagen in PE have the potential to serve as a good source of dietary supplements for the improvement of skeletal muscle mass and strength through cell protection.Keywords:branched chain amino acid, collagen, perch, skeletal muscle, sarcopenia

The Role of Vitamin D in Skeletal Muscle Repair and Regeneration in Animal Models and Humans: A Systematic Review.

Vitamin D deficiency, prevalent worldwide, is linked to muscle weakness, sarcopenia, and falls. Muscle regeneration is a vital process that allows for skeletal muscle tissue maintenance and repair after injury. PubMed and Web of Science were used to search for studies published prior to May 2023. We assessed eligible studies that discussed the relationship between vitamin D, muscle regeneration in this review. Overall, the literature reports strong associations between vitamin D and skeletal myocyte size, and muscle regeneration. In vitro studies in skeletal muscle cells derived from mice and humans showed vitamin D played a role in regulating myoblast growth, size, and gene expression. Animal studies, primarily in mice, demonstrate vitamin D's positive effects on skeletal muscle function, such as improved grip strength and endurance. These studies encompass vitamin D diet research, genetically modified models, and disease-related mouse models. Relatively few studies looked at muscle function after injury, but these also support a role for vitamin D in muscle recovery. The human studies have also reported that vitamin D deficiency decreases muscle grip strength and gait speed, especially in the elderly population. Finally, human studies reported the benefits of vitamin D supplementation and achieving optimal serum vitamin D levels in muscle recovery after eccentric exercise and surgery. However, there were no benefits in rotator cuff injury studies, suggesting that repair mechanisms for muscle/ligament tears may be less reliant on vitamin D. In summary, vitamin D plays a crucial role in skeletal muscle function, structural integrity, and regeneration, potentially offering therapeutic benefits to patients with musculoskeletal diseases and in post-operative recovery.

Vitamin D3 supplementation improves spatial memory, muscle function, pain score, and modulates different functional physiological biomarkers in vitamin D3 deficiency diet (VDD)-induced rats model

BackgroundVitamin D Deficiency is recognized as a pandemic, which is associated with high mortality. An inadequate level of vitamin D is associated with autoimmune diseases, hypertension, and cancer. The study was aimed to assess the pharmacological effects of chronic vitamin D3 supplementation on the manipulation diet regiment of deprived cholecalciferol (vitamin D3 deficient diet, VDD) rats.MethodsMemory performance (Y-maze task), muscular function (muscle grip strength), and pain score (pressure application measurement meter) were measured. Functional biomarkers were measured using ELISA method in different matrix viz. in serum (parathyroid hormone; PTH, calcitonin, thyroxine, and C-reactive protein; CRP, 25-OH Vit D3), and in CSF (klotho and β-endorphin). 25-OH Vit D3 was also estimated in liver and kidney homogenate using ELISA. Vitamin D receptor (VDR) was measured spectrophotometrically in liver and adipose tissue.ResultsVDD-induced rats showed a decrease in number of entries and time spent in the novel arm and spontaneous alternations in the Y-maze task. Significant improvements of neuromuscular function and pain score after addition of vitamin D3. In comparison to the VDD group, VDR expression (liver) and active metabolites of vitamin D3 (25-OH vit.D3) in serum were significantly higher by 48.23% and 280%, respectively. The PTH and CRP levels were significantly reduced by 32.5% and 35.27%, respectively, whereas calcitonin was increased by 36.67% compared with the VDD group. Klotho and β-endorphin expressions in cerebrospinal fluid were significantly elevated by 19.67% and 133.59%, respectively, compared to VDD group.ConclusionsOverall, the results indicate that supplementation of cholecalciferol significantly improved spatial memory impairment, VDR expression, and may provide an opportunity to manage vitamin D deficiencies.

Salbutamol ameliorates skeletal muscle wasting and inflammatory markers in streptozotocin (STZ)-induced diabetic rats

Diabetes accelerates muscle atrophy, leading to the deterioration of skeletal muscles. This study aimed to assess the potential of the β2-adrenoceptor agonist, salbutamol (SLB), to alleviate muscle atrophy in streptozotocin (STZ)-induced diabetic rats. Male Sprague Dawley rats were randomized into four groups (n=6): control, SLB, STZ (55 mg/kg, single i.p.), and STZ + SLB (6 mg/kg, orally for 4 weeks). After the final SLB dose, animals underwent tests to evaluate muscle strength and coordination, including forelimb grip strength, wire-hanging, actophotometer, rotarod, and footprint assessments. Rats were then sacrificed, and serum and gastrocnemius (GN) muscles were collected for further analysis. Serum evaluations included proinflammatory markers (tumor necrosis factor α, interleukin-1β, interleukin-6), muscle markers (creatine kinase, myostatin), testosterone, and lipidemic markers. Muscle oxidative stress (malonaldehyde, protein carbonyl), antioxidants (glutathione, catalase, superoxide dismutase), and histology were also performed. Additionally, 1H nuclear magnetic resonance serum profiling was conducted. SLB notably enhanced muscle grip strength, coordination, and antioxidant levels, while reduced proinflammatory markers and oxidative stress in STZ-induced diabetic rats. Reduced serum muscle biomarkers, increased testosterone, restored lipidemic levels, and improved muscle cellular architecture indicated SLB's positive effect on muscle condition in diabetic rats. Metabolomics profiling revealed that the STZ group significantly increased the phenylalanine-to-tyrosine ratio (PTR), lactate-to-pyruvate ratio (LPR), acetate, succinate, isobutyrate, and histidine. SLB administration restored these perturbed serum metabolites in the STZ-induced diabetic group. In conclusion, salbutamol significantly protected against skeletal muscle wasting in STZ-induced diabetic rats.

ActRIIB small molecule inhibitor 2–67 ameliorates muscle atrophy in cancer cachexia by inhibiting the myostatin/Smad pathway

Muscle atrophy is one of the major clinical features of cancer cachexia, a multifactorial complex syndrome complicated by malignancy that remains a major challenge in clinical treatment. The myostatin/Smad signaling pathway, an important pathway for muscle protein degradation, is aberrantly activated in muscle atrophy mainly by the binding of myostatin to ActRIIB kinase. Here, a series of novel small molecule compounds were screened using a molecule-level screening model for ActRIIB kinase inhibitory activity and a cell-level screening model for C26 tumor cell conditioned medium-induced C2C12 myotube atrophy. Among the compounds, compound 2–67 exhibited significant ActRIIB kinase inhibition and myotubular atrophy alleviation effects. Furthermore, 2–67 dose-dependently attenuated myocyte atrophy induced by cachexic tumor cell conditioned medium or myostatin by inhibiting the activation of the myostatin/Smad signaling pathway in C2C12 myotubes. In a C26 tumor-bearing mouse cancer cachexia model, 2–67 treatment effectively alleviated cancer cachexia symptoms. 2–67 ameliorated the loss in body weight, improved appetite, alleviated muscle loss, and preserved muscle grip strength. 2–67 also inhibited the myostatin/Smad signaling pathway in muscle tissues in cancer cachexia mice. Therefore, novel small molecule inhibitors of ActRIIB kinase may be a new option for the treatment of cancer cachexia-induced muscle atrophy, and the present work provides an important reference for the subsequent development and application of related inhibitors.

Salbutamol Attenuates Diabetic Skeletal Muscle Atrophy by Reducing Oxidative Stress, Myostatin/GDF-8, and Pro-Inflammatory Cytokines in Rats.

Type 2 diabetes is a metabolic disorder that leads to accelerated skeletal muscle atrophy. In this study, we aimed to evaluate the effect of salbutamol (SLB) on skeletal muscle atrophy in high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic rats. Male Sprague Dawley rats were divided into four groups (n = 6): control, SLB, HFD/STZ, and HFD/STZ + SLB (6 mg/kg orally for four weeks). After the last dose of SLB, rats were assessed for muscle grip strength and muscle coordination (wire-hanging, rotarod, footprint, and actophotometer tests). Body composition was analyzed in live rats. After that, animals were sacrificed, and serum and gastrocnemius (GN) muscles were collected. Endpoints include myofibrillar protein content, muscle oxidative stress and antioxidants, serum pro-inflammatory cytokines (interleukin-1β, interleukin-2, and interleukin-6), serum muscle markers (myostatin, creatine kinase, and testosterone), histopathology, and muscle 1H NMR metabolomics. Findings showed that SLB treatment significantly improved muscle strength and muscle coordination, as well as increased lean muscle mass in diabetic rats. Increased pro-inflammatory cytokines and muscle markers (myostatin, creatine kinase) indicate muscle deterioration in diabetic rats, while SLB intervention restored the same. Also, Feret's diameter and cross-sectional area of GN muscle were increased by SLB treatment, indicating the amelioration in diabetic rat muscle. Results of muscle metabolomics exhibit that SLB treatment resulted in the restoration of perturbed metabolites, including histidine-to-tyrosine, phenylalanine-to-tyrosine, and glutamate-to-glutamine ratios and succinate, sarcosine, and 3-hydroxybutyrate (3HB) in diabetic rats. These metabolites showed a pertinent role in muscle inflammation and oxidative stress in diabetic rats. In conclusion, findings showed that salbutamol could be explored as an intervention in diabetic-associated skeletal muscle atrophy.

Examining Body Fat Percentage, Galvanic Skin Response, and Muscle Grip Strength in Female Hypothyroid Patients.

Background The thyroid gland is an indispensable organ exerting control over the activity of multiple organ systems including the autonomic nervous system.This study attempted to monitor the variations in autonomic function parameters such as galvanic skin response (GSR) and muscle grip strength (HGS) in conjunction with changes in body fat percentage (BFP). Methodology This case-control study was conducted among 40 female hypothyroid patients as cases and 40 age-matched female healthy volunteers as controls. Anthropometric data were collected using standard techniques. GSR and HGS were measured using Equivital Sensory Electronic Module and Grip Force Transducer, respectively. Data extraction and analysis were done using the LabChart software. Results The mean age of the 40 female hypothyroid patients was 30.14 ± 5.91 years, whereas the mean age of the female controls was 29.37 ± 6.59 years. The waist circumference of cases was 85.81 ± 10.39 cm while that of controls was 80.90 ± 11.18 cm. The BFP of cases was 35.38% ± 6.74% while that of controls was 31.72% ± 5.63%. The GSR amplitude showed a significant difference between hypothyroid and healthy volunteers with values of 1.34 ± 1.14μS and 2.40 ± 1.86 μS, respectively. The HGS indices showed no significant difference between the two groups. A statistically negative correlation was noted between BFP and GSR amplitude (-0.32), whereas a positive correlation was noted between BFP and mean handgrip strength (0.31) in hypothyroid patients. Conclusions The changes in BFP and autonomic function through GSR and HGS were evaluated in female hypothyroid patients with respect to healthy females. The interrelationship between anthropometry and autonomic function was also explored in this study. The findings of this study can augment prognosis in patients and ensure timely corrective treatment for improving quality of life.

Nanosuspension of Foeniculum Vulgare Promotes Accelerated Sensory and Motor Function Recovery after Sciatic Nerve Injury.

The seed extract of Foeniculum vulgare (FV) was used for the preparation of a nanosuspension (NS) with an enhanced bioavailability of phytoconstituents. Subsequently, it was employed as a potent source of polyphenols, such as quercetin and kaempferol, to accelerate the regeneration and recovery of motor and sensory function in injured nerves. The NS was administered through daily gauging as NS1 (0.5 mg/mL) and NS2 (15 mg/mL), at a dose rate of 2 g/kg body weight until the end of the study. The NS-mediated retrieval of motor functions was studied by evaluating muscle grip strength and the sciatic functional index. The recovery of sensory functions was assessed by the hotplate test. Several well-integrated biochemical pathways mediate the recovery of function and the regeneration of nerves under controlled blood glucose and oxidative stress. Consequently, the NS-treated groups were screened for blood glucose, total antioxidant capacity (TAC), and total oxidant status (TOS) compared to the control. The NS administration showed a significant potential to enhance the recuperation of motor and sensory functions. Moreover, the oxidative stress was kept under check as a result of NS treatments to facilitate neuronal generation. Thus, the nanoformulation of FV with polyphenolic contents accelerated the reclamation of motor and sensory function after nerve lesion.

Long-term high loading intensity of aerobic exercise improves skeletal muscle performance via the gut microbiota-testosterone axis.

Exercise is reported to play a crucial role in skeletal muscle performance. However, the underlying mechanism is still unknown. Thus, we investigated the effect of high-intensity aerobic exercise on skeletal muscle performance. In this study, the male C57BL/6J mice were accepted by high-intensity aerobic exercise for 8 weeks to establish an exercise model. It was observed that high-intensity aerobic exercise markedly affected the expression of genes in skeletal muscle. Moreover, high-intensity aerobic exercise significantly improved skeletal muscle grip strength and serum testosterone levels. HE staining showed that the cross-sectional area (CSA) of the skeletal muscle was successfully increased after 8 weeks of high-intensity aerobic exercise. Additionally, we found that high-intensity aerobic exercise changed gut microbiota structure by altering the abundance of Akkermansia, Allobaculum, and Lactobacillus, which might be related to testosterone production. However, the beneficial effects disappeared after the elimination of the gut microbiota and recovered after fecal microbiota transplantation (FMT) experiments for 1 week. These results indicated that the beneficial effects of high-intensity aerobic exercise on skeletal muscle were partly dependent on the gut microbiota. Our results suggested that long-term high loading intensity of aerobic exercise could improve skeletal muscle performance, which was probably due to the gut microbiota-testosterone axis.

Role of Novel Polyherbal Formulations in Secondary Complications like Peripheral Neuropathy in Streptozotocin-Induced Diabetic Wistar Rats

Background: Diabetes becomes a chronic disease when glucose constantly remains high and uncontrolled. As time goes off, it may gradually develop acute or chronic associated complications. Diabetic neuropathy is one of the chronic microvascular complications, reported to affect 25% of the diabetic patient and makes patient’s life disabled and life-threatening. Hence, the present research study was designed to evaluate a novel antidiabetic polyherbal formulation, for its activity against diabetic neuropathy induced in an animal model by using streptozotocin. Materials and Methods: Novel polyherbal formulations were developed and were evaluated against streptozotocin-nicotinamide-induced diabetic neuropathy using 8–10 weeks old Wistar albino rats. Animals with diabetic neuropathy were subjected to standard neuro-protective evaluation parameters, including mechanical, chemical, and thermal tests. Results: Streptozotocin-induced hyperglycemia developed chronic neuropathic symptoms in the experimental rats between 25 - 28 days. Treatments with all four tests PHF for 8 weeks significantly improved the thermal sensation, hyperalgesia, muscle grip strength, and locomotor activity. Conclusion: By detailed research study it was revealed that out of the four polyherbal formulations studied. PHF 4 having the plant ratio of: H. sabdariffa (100): A. marmelos (50): F. religiosa (75): A. squamosa (25), the result was significantly (p &lt; 0.001) better than PHF 2, 8 and 10 (p &lt; 0.01) in reversing the symptoms of diabetic neuropathy. Thus, it was concluded that PHF 4 is excellent in treating diabetic neuropathy as well have excellent potential to prevent further progression and thus can be used against diabetic peripheral neuropathy.

Metabolites of Moringa oleifera Activate Physio-Biochemical Pathways for an Accelerated Functional Recovery after Sciatic Nerve Crush Injury in Mice.

In this study, the functional metabolites of Moringa oleifera (MO) were screened to evaluate their possible role in accelerated functional retrieval after peripheral nerve injury (PNI). MO leaves were used for extract preparation using solvents of different polarities. Each dry extract was uniformly mixed in rodents' chow and supplemented daily at a dose rate of 2 g/kg body weight from the day of nerve crush until the completion of the trial. The sciatic functional index (SFI) and muscle grip strength were performed to assess the recovery of motor functions, whereas the hotplate test was performed to measure the regain of sensory functions. An optimal level of oxidative stress and a controlled glycemic level mediates a number of physio-biochemical pathways for the smooth progression of the regeneration process. Therefore, total oxidant status (TOS), total antioxidant capacity (TAC) and glycemic levels were analyzed in metabolite-enriched extract-treated groups compared to the control. The supplementation of polar extracts demonstrated a significantly high potential to induce the retrieval of sensory and motor functions. Further, they were highly effective in controlling oxidative stress, facilitating accelerated nerve generation. This study has highlighted MO as a sustainable source of nutritive metabolites and a valuable target for drug development.

Does the objective measurement of muscle strength improve the detection of postoperative residual muscle weakness?

The postoperative residual neuromuscular block (PRNB) has a significant impact on patient safety and well-being, but continues to remain underestimated. Objective evaluation of handgrip strength using a force dynamometer can be useful to identify postoperative muscle weakness. Thirty-two American Society of Anesthesiologists (ASA) class I and II patients who received general anesthesia were included. Patients were extubated after the train-of-four (TOR) ratio (TOFR) was >0.90 and the clinical criteria for motor power recovery were judged as adequate. The measurements of handgrip strength and peak expiratory flow rate (PEFR) were obtained at baseline, 15 min after extubation, and 1, 2, and 4 h postoperatively. The incidence of significant decline from baseline (>25%) was determined. The correlation between handgrip strength and PEFR was assessed using Spearman correlation. The time to return to baseline for muscle grip strength and PEFR was performed using Kaplan-Meier survival analysis. A P value of 0.05 was considered significant for all tests. The incidence of the significant decline in handgrip strength from baseline was 100% at 15 and 60 min, 76% at 2 h, and 9.4% at 4 h. There was a strong correlation between muscle grip strength and PEFR (0.89, P < 0.001). None of the patients exhibited the potential complications of PRNB. (PRMB in abstract. It should be uniform) The mean time to return to the baseline value of muscle grip strength was 3.8 h (95% confidence interval [CI] 3.6-3.9), and the mean time to return to baseline for PEFR was 3.2 h (95% CI 2.9-3.4 h). Objective assessment of muscle grip strength using a force dynamometer has the potential to be a new objective metric to monitor postoperative muscle weakness.

Dental pulp stem cell secretome ameliorates d-galactose induced accelerated aging in rat model.

Advancing age is associated with several diseases and disorders due to multiorgan atrophy. The increasing proportion of elderly humans demands the identification of means to counteract aging and age-associated disorders. There is an increased depletion of stem cells in the aged organs, resulting in their inability to repair the damage and hence organ degeneration. Stem cell therapy has been implicated in counteracting aging and shown promise. However, the use of stem cells encounters several side effects and complications such as handling and storage of the cells for transplantation purpose. Stem cells secretome has proven to be of significant importance in a variety of disorders. In this study, we have shown that secretome derived from dental pulp stem cells (DPSCs) can reverse the age-associated degeneration induced by chronic exposure to d-galactose in a rat model. The secretome was able to increase muscle grip strength and animal activity. Secretome also improved the kidney function and hepatic biochemistry similar to healthy controls as evaluated by renal function test and Fourier-transform infrared spectroscopy. We also showed that secretome reduced the levels of monoamine oxidase and acetylcholinesterase in the brain and liver, indicating aging reversal. Finally, proteomic profiling of DPSCs secretome revealed the presence of 13 proteins which have antiaging functions. Thus, our study provides first proof of concept that DPSCs secretome can render protection against d-galactose induced accelerated aging.