Peptides derived from growth factors: Exploring their diverse impact from antimicrobial properties to neuroprotection.

Growth factor-derived peptides are bioactive molecules that play a crucial role in various physiological processes within the human body. Over the years, extensive research has revealed their diverse applications, ranging from antimicrobial properties to their potential in neuroprotection and treating various diseases. These peptides exhibit innate immune responses and have been found to possess potent antimicrobial properties against a wide range of pathogens. Growth factor-derived peptides have demonstrated the ability to promote neuronal survival, prevent cell death, and stimulate neural regeneration. As a result, they hold immense promise in the treatment of various neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis, as well as in the management of traumatic brain injuries. Moreover, growth factor-derived peptides have shown potential for supporting tissue repair and wound healing processes. By enhancing cell proliferation and migration, these peptides contribute to the regeneration of damaged tissues and promote a more efficient healing response. The applications of growth factor-derived peptides extend beyond their therapeutic potential in health; they also have a role in various disease conditions. For example, researchers have explored their influence on cancer cells, where some peptides have demonstrated anti-cancer properties, inhibiting tumor growth and promoting apoptosis in cancer cells. Additionally, their immunomodulatory properties have been investigated for potential applications in autoimmune disorders. Despite the immense promise shown by growth factor-derived peptides, some challenges need to be addressed. Nevertheless, ongoing research and advancements in biotechnology offer promising avenues to overcome these obstacles. The review summarizes the foundational biology of growth factors and the intricate signaling pathways in various physiological processes as well as diseases such as cancer, neurodegenerative disorders, cardiovascular ailments, and metabolic syndromes.

Atorvastatin ameliorates depressive behaviors and neuroinflammatory in streptozotocin-induced diabetic mice.

Depression is a chronic and progressive syndrome and commonly associated with several neuropsychiatric comorbidities, of which depression is the most studied. It has been demonstrated that statins also have anti-inflammatory and immunomodulatory properties, which being explored for potential benefits in depression. However, the role of statins in the treatment of diabetes-related depression has not been well examined. Herein, we investigated the effects of atorvastatin on depressive behaviors and neuroinflammation in streptozotocin-induced diabetic mice. Our data indicated that oral administration of atorvastatin at 10 or 20 mg/kg for 3 weeks markedly ameliorated diabetes-associated depressive behaviors reflected by better performance in sucrose preference test (SPT), tail suspension test (TST), and novelty-suppressed feeding test (NSFT). The study further showed that atrovastatin decreased the expression of nucleus NF-κB p65 expression and ameliorated neuroinflammatory responses in prefrontal cortex as evidenced by less Iba-1-positive cells and lower inflammatory mediators including IL-1ß and TNF-α. As expected, atorvastatin-treated diabetic mice exhibited significant improvement of hyperlipidemia rather than hyperglycemia. These results suggest that atorvastatin has the potential to be employed as a therapy for diabetes-related depression.

Dynamic changes in eosinophilic inclusion bodies in lactacystin-incubated PC12 cells / 中华神经医学杂志

Objective To explore the development of eosinophilic inclusion bodies in PC12 cells incubated with proteasome inhibitor lactacystin. Methods PC12 cells were incubated for 24 h with 0, 5, 10 and 20 μmol/L lactacystin, and HE staining and α-synuclein immunohistochemistry was used to observe the changes of the inclusion bodies under light microscope. The changes in the inclusion bodies in the cytoplasm were also observed after treatment of PC12 cells with 10 μmol/l lactacystin for 24, 48, 72, 96 and 120 h. Results After incubation with lactacystin for 24 h, P12 cells showed increased number of eosinophilic inclusion bodies in the cytoplasm, and the increment appeared dose dependent. No inclusion bodies were observed in the cells without lactacystin treatment, and a few (3.33%±1.15%) occurred at lactacystin concentration of 5 μmol/L, numerous (71.33%±4.16%) at 10 μmol/l, and almost in every cell (90.33%±3.21%) at 20 μmol/L; some of the inclusion bodies were released from the cells. With the passage of time, inclusion bodies in the cells treated with 10 ?mol/l laetacystin began to dissociate with the cells, and the cytoplasm was reduced to contain only inclusion bodies and nucleus at 96 and 120 h. Immunohistochemistry showed that a -synuclein immunoreaetive granules concentrated and formed inclusion bodies close to the nucleus at 24 h. As the concentration increased and time prolonged, α-synuclein-immunoreactive inclusion bodies were released from the cells, leaving only inclusion bodies and cell nuclei presented at 96 and 120 h. Conclusion Incubation with laetacystin can induce cytoplasmic eosinophilic and α-synuclein-immunoreaetive inclusion bodies in PC12 cells. The development of inclusion bodies in this model is consistent with that in human Parkinson's disease and diffused Lewy body disease. This model is helpful for further study of the mechanism of neurodegenerative diseases.

Epidemiological survey of the association between non alcoholic fatty liver disease and metabolic syndrome in civil servants of Chongqing city / 中华预防医学杂志

<p><b>OBJECTIVE</b>To investigate the association between non alcoholic fatty liver disease (NAFLD) and metabolic syndrome (MS).</p><p><b>METHODS</b>A cross-sectional multiple-stage stratified survey was performed. A total of 2190 civil servants of Chongqing city were invited to participate in the survey covering physical examination, serum biochemistry-profile and ultrasonographic examination of liver.</p><p><b>RESULTS</b>Of 2176 valid questionnaires, altogether 455 cases were diagnosed as NAFLD and 231 individuals were diagnosed as MS. The prevalence of obesity, hyperglycemia, blood lipid disturbance, primary hypertension, NAFLD and MS was 38.3%, 5.5%, 31.7%, 29.9%, 20.9% and 10.6% respectively, which was increased along with aging (chi2 = 31.775, P = 0.000; chi2 = 25.985, P = 0.000; chi2 = 44.818, P = 0.000; chi2 =149.802, P = 0.000; chi2 = 61.302, P = 0.000; chi2 = 43.508, P = 0.000 a partly). The prevalence of obesity, hyperglycemia, dyslipidemia, primary hypertension, metabolic syndrome was significantly higher than those in control group (chi2 = 384.554, P = 0.000; chi2 = 25.597, P = 0.000; chi2 = 370.849, P = 0.000; chi2 = 40.252, P = 0.000; chi2 = 215.077, P = 0.000 separately), and the level of body mass index (BMI), fasting plasma glucose (FPG), triglyceride (TG), systolic blood pressure (SBP), diastolic blood pressure (DBP) in NAFLD group was remarkably higher than those in control group (t = 26.308, P = 0.000; t = 6.055, P = 0.000; t = 15.980, P = 0.000; t = 10.550, P = 0.000; t = 13.628, P = 0.000 respectively), while the level of high-density lipoprotein cholesterol (HDL-C) was on the opposite (t = 20.067, P = 0.000). Compared with the control group, odds risk for NAFLD was 22.82 folds (95% CI: 12.64-41.19) in obesity, 20.97 folds (95% CI: 11.21-39.24) in hyperglycemia, 24.40 folds (95% CI: 13.51-44.07) in dyslipidemia, 15.73 folds (95% CI: 8.66-28.60) in primary hypertension, while the risk for NAFLD was the highest in MS (OR = 31.06, 95% CI: 17.12-56.35). There were simple or multiple metabolic disorders in 455 individuals diagnosed as NAFLD, and 21 case (4.6%) with obesity, hyperglycemia, dyslipidemia and primary hypertension.</p><p><b>CONCLUSION</b>NAFLD is closely related with MS, which may be considered as a feature of MS.</p>